LIBRARY 

OF    THE 

UNIVERSITY  OF  CALIFORNIA. 


CUsS       BIOLOGY 
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I.     Bacteria. 


II.     Fungi. 


III.     Protozoa. 


CAUSES  OF  INFECTIOUS  DISEASES. 


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THE  PATHOLOGY 


AND 


DIFFERENTIAL  DIAGNOSIS 


OF 


INFECTIOUS  DISEASES  OF  ANIMALS 


By  VERANUS  ALVA  MOORE,  B.S.,  M.D. 

Professor  of  Comparative  Pathology,  Bacteriology  and  Meat 

Inspection,   New  York  State  Veterinary  College, 

Cornell    University,  Ithaca,   N.  Y. 


WITH    AX    INTRODUCTION'    BY 


VERSJTY 


DANIEL  ELMER  SALMON,  D.V.M. 

Chief  of  the  Bnreau  of  Animal  Indnstry,   United  States 
Department  of  Agriculture. 


ILLUSTRATED. 


ITHACA.  N.  Y.  : 

TAYLOR    &    CARPENTER. 

1902. 


PRESS    OF 

JOURNAL    JOB    DEPARTMENT 

ITHACA,     N.    Y. 


Copyright,   1902. 
By  Veranus  Alva  Mookk. 


GENERAL 


TO  DANIEL  ELMER  SALMON 

LARGELY  THROUGH  WHOSE  LABORS  THERE  WAS  ES- 
TABLLSHED  LX  THE  UNITED  STATES  DEPARTMENT  OF 
AGRICULTURE  THE  BUREAU  OF  ANIMAL  INDUSTRY 
WHICH  HAS  MADE  POSSIBLE  EXTENSIVE  INVESTIGA- 
TIONS INTO  THE  NATURE  OF  EPIZOOTIC  DISEASES  IN 
AMERICA  AND  WHO  FOR  EIGHTEEN  YEARS  HAS  DI- 
RECTED   THESE    INVESTIGATIONS 

THIS  VOLUME  IS  DEDICATED. 


1022G7 


PREFACE. 


The  literature  on  infection  and  the  etiology  and  morbid 
anatomy  of  infectious  diseases  of  animals  is  exceedingly  rich  in 
the  results  of  new  discoveries  and  important  investigations. 
However,  students  just  beginning  this  study  and  following  a 
prescribed  curriculum  have  not  the  time  nor  are  they  prepared  to 
read  with  profit  the  detailed  records  of  original  research.  Such 
publications  seem  to  be  better  adapted  for  those  doing  advanced 
or  graduate  work.  Furthermore,  many  of  these  publications  are 
out  of  print  and  are  only  available  for  consultation.  For  these 
reasons  it  is  believed  that  a  volume  containing  the  rudiments 
of  the  subject  will  be  of  use  to  the  student  and  an  aid  to  the 
teacher.  It  is  also  believed  that  such  a  work  will  be  of  assistance 
to  practitioners. 

In  preparing  this  volume  the  aim  has  been  to  bring  to- 
gether in  a  concise  form  the  fundamental  facts  in  the  path- 
ology of  the  more  common  infectious  diseases  of  animals, 
especially  those  existing  in  the  United  States,  with  which 
sanitarians  and  the  practitioners  of  comparative  medicine  must 
contend.  To  this  end,  the  current  literature,  the  reports  of 
the  investigations  made  at  various  Institutions  and  Experi- 
ment Stations,  as  well  as  the  standard  works  on  comparative 
pathology  have  been  freely  drawn  upon  and  to  all  of  w^hich 
full  acknowdedgment  is  hereby  made. 

In  order  to  bring  into  consideration  the  clinical  value  of  a 
knowledge  of  morbid  anatomy,  a  few  of  the  symptoms  or  ante- 
mortem  manifestations  have  been  included.  It  is  hoped  that 
this  correlation  of  symptoms  and  lesions  will  stimulate  a  deeper 


VI  PREFACE 

interest  in  the  stud}'  of  comparative  patholog}-  and  thus  render 
it  of  more  permanent  and  practical  value  for  those  entering 
into  the  practice  of  veterinary  medicine. 

In  selecting  the  subject  matter  care  has  been  taken  to 
avoid,  as  far  as  possible,  the  introduction  of  results  concerning 
which  there  are  controversies.  It  has  seemed  best  to  deal 
with  those  facts  about  which  at  the  present  time  there  is  little 
or  no  doubt.  After  the  discussion  of  each  disease  a  few  refer- 
ences to  the  literature  are  appended.  These  are  intended  sim- 
ply to  bring  the  attention  of  the  student  to  a  few  publications 
respecting  the  cause  and  morbid  anatomy,  considered  in  the 
light  of  modern  etiology,  of  the  disease  in  question  and  to  a 
few  articles  containing  the  results  of  original  research. 

In  order  not  to  complicate  or  unnecessarily  expand  this 
text,  a  knowledge  of  general  pathology  and  the  principles  of 
bacteriology  has  been  taken  for  granted. 

The  difficulties  involved  in  the  preparation  of  such  a  text 
are  both  numerous  and  obvious.  The  indication  of  errors  or 
omissions  with  any  other  criticisms  that  will  tend  to  better 
the  volume  and  increase  its  efficiency  for  the  student  will  be 
thankfully  received. 

V.  A.  M. 


TABLE  OF  CONTENTS. 


PAGE 

List  of  Iixustrations ix 

List  OF  Reference  Books xi 

Introduction '^^ 

CHAPTER  I. 

General  consideration  concerning  etiology,  infection  and 
SPECIFIC  INFECTIOUS  DISEASES.  (  Etiology,  Infection,  Channels 
of  infection.  Wound  infection,  Bacteria  causin.<;  wound  infec- 
tion, Lesions  presumably  of  wound  infection  origin  that  are 
recognized  as  distinct  maladies,  Botryomycosis,  Omphalophle- 
bitis, White  scours.  Infectious  suppurative  cellulitis,  Fistulous 
withers  and  poll-evil,  Infectious  mastitis,  A  specific  infectious 
disease,  The  differential  characters  of  a  specific  infectious 
disease.  Cause  for  the  variation  in  the  course  of  an  infectious 
disease.  Grouping  of  specific  infectious  diseases) i 

CHAPTER  II. 

Diseases  caused  by  streptococci 27 

General  discussion  of  streptococci 27 

Strangles 33 

Equine  contagious  pleuro-pneumonia . 37 

Apoplectiform  septicaemia  in  chickens 44 

CHAPTER  III. 

Diseases  caused  by  bacteria— genus  bacterium 47 

Swine  plague •  47 

Hemorrhagica  septicaemia  in  cattle 68 

Fowl  cholera 77 

Anthrax ^^ 

Infectious  leukaemia  in  fowls 9^ 

Swine  erysipelas I07 

Glanders "3 

Tuberculosis ^27 

Ovine  caseous  lymph-adenitis 161 

Asthenia 167 


Vlll  CONTENTS 

CHAPTER  IV. 

Diseases  caused  by  bacteria — genus  bacili^us 169 

Hog  cholera 169 

Tetanus 185 

Symptomatic  anthrax 195 

CHAPTER  V. 

Diseases  caused  by  higher  fungi 204 

Actinomycosis 204 

Leeches 218 

Pneumomycosis 228 

CHAPTER  VI. 

Diseases  caused  by  protozoa 236 

Texas  fever , 236 

Infectious  entero-hepatitis  in  turkeys 252 

Surra 265 

Dourine 274 

CHAPTER  VII. 

Infectious  diseases  for  which  the  specific  cause  is  not  yet 

determined 282 

Rinderpest 282 

Contagious  pleuro-pneumonia  in  cattle 290 

Foot  and  mouth  disease 302 

Rabies 306 

Diphtheria  in  fowls 325 

Influenza 334 

Dog  distemper 340 

Infectious  cerebro-spinal  meningitis 347 

Cornstalk  disease  in  cattle 349 

CHAPTER  VIII. 

A  FEW  diseases  caused  BY  ANIMAE  PARASITES 355 

The  nodular  disease  of  the  intestines  of  sheep  and  cattle 355 

Nodular  taeniasis  in  fowls 360 

Trichinosis 364 

APPENDIX. 

Disinfection 370 


ILLUSTRATIONS. 


PLATES. 


Bacteria,  fungi  and  protozoa Frontispiece 

Tuberculous  bovine  heart II 

Tuberculous  and  healthy  spleens,  pig III 

Tuberculosis  of  lung,  pig I^ 

Fungus  associated  with  leeches V 

Aspergillar  pneumonia ^T 

Map  showing  Texas  fever  line VII 

Diphtheria  in  pigeons ^  HI 


FIGURES  IX  TEXT. 

PAGE 

1.  Streptococcus  of  mastitis i6 

2.  Section  of  cow's  udder I7 

3.  Abscess  in  partially  immunized  rabbit 23 

4.  Morphology  of  streptococcus 28 

5.  Bacterium  of  swine  plague 4^ 

6.  Lung  with  interlobular  lymph  infiltration 53 

7.  Lung  showing  emphysema  in  interlobular  spaces 54 

8.  Right  lung  of  pig  showing  areas  alTected  with  swine  plague...  55 

9.  Portion  of  lung  showing  hemorrhagic  interlobular  infiltration  .  58 

10.  Anthrax  bacteria  from  an  impression  preparation 83 

11.  Bacteriinii  anthracis 84 

12.  Cover-glass  preparation  from  anthrax  blood 85 

13.  Bacieriicm  saiiguinarium 99 

14.  Bacterium  sanguinarium  in  the  liver 99 

15.  Temperature  chart  of  fowl  affected  with  leukaemia 100 

16.  Diseased  blood  in  infectious  leukaemia 102 

17.  Congested  liver  in  infectious  leukaemia 103 

18.  Phagocytic  action  of  leucocytes  on  the  red  blood  corpuscles..  104 

19.  Bacterium  of  swine  erysipelas 108 

20.  Bacteriut)i   mallei nS 

21.  Xasal  septum,  glanders 118 

22.  Farcy,  cutaneous  glanders 120 

23.  Bacterium   tuberculosis 131 

24.  Lymph  glands  on  side  of  cow's  head 137 

25  Dorsal  aspect  of  bovine  lungs 138 

26.  Bovine  tracheal  and  bronchial  lymph  glands 139 

27.  Posterior  mediastinal  glands 140 

28.  Suppurating  tubercular  focus,  cow's  lung —  141 

29.  Tuberculous  omentum,  cow. 142 


X  ILLUSTRATIONS 

30.  Small  tubercular  nodules,  parietal  pleura,  cow 143 

31.  Beginning  tubercle  in  spleen 145 

32.  Section  of  tuberculous  lung,  cow 146 

33.  Tuberculous  spleen,  pig 155 

34.  Chart  showing  the  effect  of  cold  water  on  temperature 157 

35.  Non-tubercular  temperature  reaction 15S 

36.  Chart  showing  tuberculin  reaction 159 

37.  Bacterium  of   Preisz 162 

38.  Bactej-JKui  asiheniae 167 

39.  Bacillus  of  hog  cholera 171 

40.  Ulcerated  intestine  in  hog  cholera 176 

41.  Spleen  of  pig,  normal  and  with  hog  cholera 177 

42.  Bacillus  tetani 186 

43.  Bacillus  of  symptomatic  anthrax 197 

44.  Ray  fungus 206 

45.  Actinomycosis,  head  of  steer 210 

46.  Section  of  actinomycotic  jaw 211 

47.  Actinomycosis  of  upper  jaw 212 

48.  Actinomycosis  in  tongue 213 

49.  Leeches,  lesions  in  lip  of  horse 222 

50.  Leeches,  lesions  in  lip  of  horse 223 

51.  Isolated  nodule  from  lesion 223 

52.  Club-like  ends  of  hj-phae  fungus,  "leeches" 224 

53.  Section  through  nodule,  "leeches" 225 

54.  Piroplasina  bigeininiiui.    . 23S 

55.  Coccus  form  of  Piroplasma  bigeminum 239 

56.  Texas  fever  parasite  in  blood  of  kidney 239 

57.  Coccus  form  of  Texas  fever  parasite  in  kidney 240 

58.  Capillary  of  heart  showing  invasion  of  corpuscles  with  Piro- 

plasma bigeminum 240 

59.  Adult  male  tick,  Boophilus  bovis 241 

60.  Bull  suffering  from  Texas  fever 242 

61.  Adult  female  tick,  Boophilus  bovis 243 

62.  Eggs  and  young  tick,  Boophilus  bovis 243 

63.  Amoeba   meleagridis 254 

64.  Caeca  of  turkey  with  lesions  of  entero-hepatitis 258 

65.  Caecum  showing  ulcers  in  entero-hepatitis 259 

66.  Liver  of  turkey  affected  with  entero-hepatitis 260 

67.  Trypanosoma  Evansi 266 

68.  Photograph  of  Trypanosoma  in  blood 267 

69.  Nodular  disease  in  sheep,  cross  section  of  intestine 355 

70.  Cross  section  of  worm  nodule 358 

71.  Taeniasis  in  chickens 362 

72.  Sectioi:s  showing  nodule  and  worm 363 

73.  Encapsuled  Trichinella  spiralis 365 


A  LIST  OF  REFERENCE  BOOKS. 


BouLEV  ET  Reynal. — Nouveau  Dictionnaire  pratique  de   Medecine  de 

Chirurgie  et  d'H3'giene  Veterinaires. 
C ADEAC.  — Encyclopedie  Veterinaire. 

DiECKERHOFF.— Lehrbuch  der  Speciellen  Pathologic  und  Therapie  fiir 

Thierarzte. 
EttENBERCER,  SCHUTz  UND  Baum.— Jahresbericht  iiber  die  Leistungen 

auf  dem  Gebiete  der  Veterinar-Medicin. 
Fleming. — A  manual  of  veterinary  sanitary  science  and  police. 

Friedberger  und  Frohxer. — Lehrbuch  der  Speciellen  Pathologie  u. 

Therapie  der  Hausthiere. 
GalTier. — Traite  des  Maladies  Contagieuses  et  de  la  Police  Sanitaire  des 

Aniniaux  domestiques. 
KiTT. — Lehrbuch  der  Pathologischen  Anatomie  der  Hausthiere. 

Law. — Veterinary  Medicine. — (Especially  Vol.  IV.) 

LUBARSCH  UND  OSTERTAG.— Ergebuisse  der  Allgenieinen  Pathologie  und 
Pathologischen  Anatomie  des  Menschen  und  der  Tiere. 

OSTERTAG. — Handbuch  der  Fleischbeschau  fiir  Tierarzte,  Arzte  und 
Richter. 

Reynal. — Traite  de  la  Police  Sanitaire  des  Animaux  Domestiques. 

ScHNEiDEMiJHi,.— Lehrbuch  der  vergleichenden  Pathologie  und  Therapie 

des  Menschen  und  der  Hausthiere. 
Walley. — The  four  bovine  scourges. 


For  bibliography  on  all  medical  subjects,  see  Index-catalogue  of  the 
library  of  the  Surgeon-General's  office. 

Annual  Reports,  Special  Reports  and  Bulletins  on  Animal  Diseases 
issued  by  the  Bureau  of  Animal  Industry,  LT.  S.  Department  of  Agricul- 
ture, Washington,  D.  C. 

Proceedings  of  the  American  Veterinary  Medical  Association. 

The  Bulletins  on  Animal  Diseases  issued  by  the  various  State  Agri- 
cultural Experiment  Stations. 


INTRODUCTION. 


An  elementary  treatise  on  the  pathology  of  the  infectious 
diseases  of  animals — a  treatise  that  states  briefly,  clearly  and 
comprehensively  all  that  is  known,  and  excludes  all  that  is 
not  known—has  long  been  needed  not  only  by  the  students 
who  are  beginning  this  interesting  subject,  but  by  members 
of  the  veterinary  profession  who,  as  practitioners,  investigators 
or  teachers,  wish  to  learn  in  the  shortest  time  the  present  con- 
dition of  our  knowledge.  A  work  which  supplies  this  need 
will  be  welcomed  and  appreciated. 

There  are  few  subjects  more  important  to  Americans  than 
a  thorough  comprehension  of  the  infectious  diseases  of  animals. 
An  enormous  amount  of  money  is  invested  in  the  domesticated 
animals  in  the  United  States,  and  the  .security  of  this  invest- 
ment depends  very  largely  upon  our  ability  to  protect  these 
animals  from  infectious  diseases.  There  are  ma'ny  diseases  of 
this  class  which  spread  among  animals  as  smallpox,  bubonic 
plague  or  cholera  spread  among  mankind  ;  and  it  requires  a 
thorough  knowledge  of  all  the  characteristics  of  such  diseases 
to  guard  against  them,  to  recognize  them  when  they  appear  or 
to  control  them. 

For  a  period  already  too  long,  exact  knowledge  of  these 
diseases  has  been  confined  to  a  comparatively  small  number  of 
men  ;  but  with  the  great  property  interests  at  stake  it  is  ex- 
tremely desirable  that  this  information  should  be  distributed, 
that  not  only  responsible  officials  but  every  practitioner  should 
share  it.  With  not  far  from  three  thousand  million  dollars 
worth  of  farm  animals  in  this  country,  and  with  a  single  disease 


INTRODUCTION  Xlli 

that  sometimes  destroys  a  hundred  million  dollars  worth  of 
property  in  a  year,  it  is  not  difficult  to  see  the  value  of  that 
precise  knowledge  which  is  required  to  deal  promptly  and 
efficiently  with  these  plagues. 

It  is  a  narrow  and  incorrect  view  to  hold  that  the  farmer 
who  owns  these  animals  is  the  only  one  who  suffers  from  the 
ravages  of  the  diseases  which  destroy  them.  Animal  products 
constitute  a  large  part  of  the  national  food  supply.  If  this  food 
supply  is  diminished,  made  dearer  and  more  difficult  to  obtain, 
want,  misery,  disease  and  death  among  mankind  increase.  At 
first  the  effects  of  a  scarcity  of  the  food  supply  may  be  almost 
inappreciable  and  felt  only  by  the  very  poor  ;  but  as  the  con- 
ditions of  famine  are  approached,  suffering  is  multiplied  and 
intensified  until  whole  communities  are  prostrated  or  destro^-ed. 
An  abundant  supply  of  wholesome  and  nutritious  food  is,  there- 
fore, an  essential  condition  of  the  welfare  and  prosperity  of  a 
people. 

The  great  commercial  operations  of  nations  also  depend  to 
a  great  extent  upon  the  good  condition  of  animals.  When 
all  of  the  horses  are  disabled  by  an  epizootic,  as  they  have 
been  on  rare  occasions  by  influenza,  the  delivery  of  purchased 
goods  has  nearly  ceased,  the  shipments  of  flour,  iron,  machinerj^ 
and  other  products  have  been  temporarily  arrested  and  busi- 
ness has  been  almost  at  a  standstill.  Again,  it  should  be  re- 
membered that  we  export  annually  from  the  United  States 
forty  million  dollars  worth  of  live  animals,  one  hundred  million 
dollars  worth  of  meats,  fifty-five  million  dollars  worth  of  lard, 
tallow  and  other  animal  fats,  and  nine  million  dollars  worth 
of  dairy  products.  Let  this  traffic  be  stopped  by  a  shortage 
of  supplies  or  by  prohibitive  orders  of  other  nations  on  account 
of  the  unrestrained  prevalence  of  infectious  diseases,  and  the 
earnings  of  steamships,  and  rail-roads,  and  banks,  and  com- 
mission houses,  are  at  once  diminished  ;  men  employed  in  these 


XIV  INTRODUCTION 

enterprises  are  discharged,  and  in  innumerable  ways  the  wel- 
fare of  people  who  have  no  part  in  the  ownership  of  any  of 
these  animals  or  their  products  is  affected. 

Finally  the  most  serious  of  all,  is  the  case  in  which  the 
animal  plague,  in  addition  to  being  destructive  to  animal  life, 
is  communicable  to  and  fatal  to  man,  as  is  true  of  anthrax, 
rabies  and  tuberculosis.  Such  diseases  destroy  property,  dis- 
turb business,  lessen  the  food  supply,  and  directly  threaten 
human  life.  What  more  is  needed  to  impress  upon  the  reader 
the  supreme  importance  of  studying  and  understanding  the 
infectious  diseases  of  animals  ? 

The  pathology  of  these  diseases  is  in  itself  a  large  subject. 
Investigations  concerning  it  have  extended  over  more  than  a 
century  of  time  and  the  literature  of  the  subject  is  enormous. 
To  concentrate  this  knowledge,  to  select  the  truth  and  discard 
the  errors,  and  to  develop  a  concise  and  sj^stematic  treatise  is 
a  task  of  great  magnitude  and  one  which  has  required  much 
labor  and  thought.  The  writer  has  not  seen  the  manuscript, 
but,  from  his  long  and  intimate  acquaintance  with  the  author, 
he  feels  sure  that  the  work  has  been  patiently,  carefully,  intelli- 
gently and  thoroughh'  done,  and  that  it  will  be  favorably 
received. 

D.  E.  Salmon. 


CHAPTER  I. 

GENERAL    CONSIDERATION    OF     ETIOLOGY,    INFECTION 
AND    SPECIFIC    INFECTIOUS   DISEASES. 


§  I.  Etiology.  The  development  of  the  science  of  bac- 
teriology, together  with  a  knowledge  of  the  parasitic  protozoa, 
has  demonstrated  that  a  large  number  of  the  infectious  dis- 
eases are  the  direct  result  of  the  invasion  of  the  animal  body  by 
certain  species  of  microorganisms.  A  specific  etiology  which 
teaches  that  for  each  of  the  various  epizootics  we  have  a  sin- 
gle, definite  cause  has  become  recognized  and  accepted  by  all 
pathologists.  Although  there  are  a  number  of  distinct  diseases 
for  which  such  a  specific  agent  has  not  been  found,  the  evi- 
dence in  the  very  nature  of  the  maladies,  is  conclusive  that  for 
each  of  these  such  an  etiological  factor  exists. 

In  studying  the  pathology  of  infectious  diseases  the  idea 
of  a  definite  and  adequate  cause  should  be  kept  in  mind.  It  is 
no  longer  justifiable  to  attribute  them  to  an  unfavorable  en- 
vironment, poor  hygiene,  or  improper  sanitation,  conditions 
which  may  aid  the  specific  cause  but  which  cannot  supplant 
it.  It  is  often  a  troublesome  task  to  differentiate  between  the 
morbid  affections,  often  fatal  in  their  results,  brought  about  by 
improper  care  and  food,  and  the  maladies  dependent  upon  a 
specific  cause.  The  reason  why  many  of  the  former  theories 
accepted  unsanitary  conditions,  certain  kinds  of  food  or  other 
similar  agencies  as  the  etiology  of  distinct,  infectious  diseases, 
is  found  in  the  fact  that  the  infectious  microorganisms  were 
and  still  are  often  transmitted  to  the  individual  through  such 
channels.  It  is  important,  therefore,  that  the  limitations  of 
both  the  exciting  cau.se  and  the  environment  .should  be  fully 
taken  into  account.  Although  for  certain  diseases  such  as 
rinderpest  and  rabies  we   do   not   know  just  what  the  specific 


2  ETIOLOGY 

cause  is,  the  fact  that  its  location  in  the  body  of  the  diseased 
animal  is  known,  that  with  these  morbid  tissues  the  disease  can 
be  produced  in  healthy  animals  and  that  without  these  definite 
infections,  no  matter  what  the  surroundings  are,  they  cannot 
be  made  to  develop,  argues  against  extraneous  conditions  as 
exciting  causes. 

The  mysteries  which  formerly  surrounded  the  origin,  the 
course  and  the  disappearance  of  animal  plagues  have  in  a  large 
degree  been  cleared  awa}-  and  in  their  place  we  are  con- 
fronted with  the  problems  involved  in  the  life  history  and  the 
possibilities  of  invading  microorganisms.  In  fact  during  the 
last  few  years  the  biological  sciences  have  been  brought  into 
immediate  use  by  the  pathologist.  Etiology  has  become  per- 
manently linked  to  microbiology  so  that  in  seeking  for  the 
specific  cause  of  an  infectious  disease  we  look  for  some  spe- 
cies of  organic  life  which  may  belong  either  to  the  animal  or 
to  the  vegetable  kingdom.  The  fact  that  certain  animals  and 
plants  have  become,  if  the}'  were  not  in  the  beginning,  para- 
sitic on  other  larger  and  higher  forms  of  life  has  long  been 
recognized,  but  the  idea  came  later,  that  the  various  infections 
giving  rise  to  a  wide  series  of  phenomena,  known  as  symptoms 
and  morbid  anatomy,  were  actually  and  simply  the  results  of 
the  invasion  of  the  individual  with  living  microscopic  plants 
(bacteria)  or  animals  (protozoa J.  It  is  likewise  true  that  for 
many  of  the  disorders  consisting  of  changes  recognized  in  the 
terms  of  general  pathology,  the  cause  may  be  found  in  the  con- 
ditions of  life  under  which  the  individual  has  been  forced  to 
exist.  Etiology,  therefore,  in  a  broad  sense,  includes  both  the 
infecting  or  parasitic  microorganisms  which  cause  infections 
and  produce  the  specific  infectious  diseases  and  poor  hygienic, 
unsanitar}'  conditions  and  physical  forces  which  maj-  produce 
non-specific  morbid  changes  often  sufficient  to  cause  death. 

§  2.  Infection.  The  term  infection  has  come  to  be  gen- 
erally understood  to  mean  the  entrance  into  the  animal  body, 
from  without,  of  living  microorganisms  capable  of  multiplying 
within  the  living  tissues  and  of  producing  in  consequence 
thereof  a  local  or  a  general  diseased  condition  or  the  death  of  the 
individual.     The  invading  microorganisms  may  belong  to  any 


INFECTION  ^ 

one  of  the  three  great  groups  of  microscopic  hfe,  namely,  bac- 
teria, higher  fungi,  or  protozoa.  It  is  customary  and  convenient, 
if  not  altogether  logical,  to  limit  the  term  microorganism  to  these 
forms  excluding  altogether  the  entozoa  and  other  animal  para- 
sites most  of  which  are  not  microscopic  in  size. 

A  diseased  condition  produced  by  substances  not  capable  of 
reproducing  themselves  as,  for  example,  organic  or  inorganic 
chemical  compounds,  is  an  intoxicative  process.  In  an  infection, 
the  immediate  cause  of  the  symptoms  and  morbid  changes  in 
the  tissues  is  an  intoxication  due  to  the  action  of  the  metabolic 
products  (toxins)  of  the  invading  microorganisms.  The  the- 
ories of  their  mechanical  interference  with  the  normal  functions 
of  the  body  or  that  they  absorb  the  nutriment  thus  depriving 
the  tissues  of  necessary  food  wait  for  demonstration.  The  re- 
sults of  infection  vary  in  their  manifestations.  If  the  invading 
organisms  remain  at  the  point  of  entrance  and  produce  local 
tissue  changes,  the  condition  is  spoken  of  as  a  wound  mfedion  ; 
if  the  invading  bacteria  become  widely  distributed  in  the  cir- 
culation and  tissues,  the  condition  is  known  as  septicaemia  ;  if 
the  infecting  bacteria  remain  at  the  point  of  entrance,  multiply 
there  elaborating  a  toxin  which  is  absorbed  and  which  causes 
symptoms  and  possibly  death,  the  condition  is  a  toxaemia; 
if  the  invading  organism  happens  to  be  that  of  a  specific  dis- 
ease, such  as  the  bacterium  of  anthrax,  giving  rise  to  a  defin- 
ite series  of  symptoms  and  lesions,  the  affection  is  designated 
a  specific,  infectious  disease.  Through  the  agency  of  metas- 
tasis, invading  microorganisms  may  be  carried  from  the  point 
of  introduction  to  other  parts  of  the  body  where  they  may  be- 
come localized,  multiply  and  give  rise  to  any  one  of  many 
forms  of  lesions.  It  may  happen  that  the  point  of  entrance  is 
so  obscure  that  the  resulting  morbid  changes  are  not  easily 
traced  to  an  external  infection.  There  are  many  illustrations 
of  this  in  comparative  pathology  such,  for  example,  as  suppur- 
ative cellulitis.  For  convenience  in  discussion,  infections  may 
be  divided  into  the  two  clinical  groups,  namely,  wound  infec- 
tions and  specific  infectious  diseases  although  in  certain  in- 
stances they  cannot  be  separated. 


4  INFECTION 

In  arriving  at  a  clear  understanding  of  the  nature  of  in- 
fections, it  is  well  not  to  be  too  closely  circumscribed  by 
classifications.  It  is  better  to  look  upon  them  as  a  series  of 
processes  going  on  in  the  animal  world  due  to  the  activities  of 
infecting  or  parasitic  microorganisms.  In  other  words,  the 
lesions  following  an  infection  or  a  specific  infectious  disease 
are  simply  the  results  of  parasitism. 

In  the  study  of  the  various  forms  of  infection  in  the  lower 
animals,  lesions  have  been  found  to  contain,  apparentlj^  as  their 
causative  factors,  bacteria  which  suggest  at  least  that  certain  of 
the  supposed  saphrophytic  organisms  ma5^  under  certain  con- 
ditions, become  parasitic  and  cause  infections  resulting  in  more 
or  less  local  or  generalized  disturbance.  Many  lesions  seem  to 
be  produced  by  bacteria  which  are  harbored  normally  upon 
the  skin.  When  these  organisms  are  introduced  by  accident 
into  the  living  tissues  they  multiply  and  acquire,  if  they  did 
not  already  possess  it,  the  power  to  produce  tissue  changes. 
We  cannot,  therefore,  dismiss  the  subject  of  infection  without 
a  passing  consideration  of  the  possible  etiological  significance, 
under  certain  conditions,  of  many  ordinarily  considered  harm- 
less species  of  bacteria  with  which  the  animal  body  is  con- 
stantly surrounded.  In  the  search  for  the  cause  of  many  le- 
sions supposed  from  their  nature  to  be  infectious,  or  in  apply- 
ing methods  for  their  prevention,  it  is  well  to  take  into  consid- 
eration all  microorganisms  which  might  possibly  be  the  caus- 
ative factors  and  not  limit  the  search  to  the  detection  of  the 
already  recognized  pathogenic  species.  Recent  investigations 
point  to  the  conclusion  that  frequently  domesticated  animals 
suffer  as  the  result  of  the  invasion  of  bacteria  at  present  not 
listed  among  the  pathogenic  microorganisms,  and  what  is  true 
in  this  regard  for  bacteria,  may  be  hypothetically  applied  to 
the  higher  fungi  and  to  the  protozoa. 

§  3.  Channels  of  Infection.  There  are  a  number  of 
ways  by  which  microorganisms  may  be  introduced  into  the 
living  tissues  of  the  animal  body.  The  more  common  of  these 
areas  follows,  namely  : 

(  I  )  Through  the  digestive  tract.  Bacteria  gain  entrance 
into  the  tissues  from  the   digestive  tract  where  thev  have  been 


CHANNELS    OF    INFECTION  5 

brought   with   the   food  or  water.      Hog  cholera  infection  is  a 
good  ilhistration  of  this  mode  of  entrance. 

(  2  )  Through  the  respiratory  tract.  Bacteria  are  taken  into 
the  hmgs  where  they  are  brought  with  the  inhaled  atmosphere. 
Pulmonary  tubercular  affection  is  often  brought  about  in  this 
way. 

(3)  Throu^li  abrasions  of  the  skin.  The  wide  distribu- 
tion of  bacteria  in  nature  renders  it  highty  probable  that  in  all 
wounds  of  the  integument  microorganisms  will  reach  the  fresh 
tissues.  They  maj-  come  from  the  cutting  or  tearing  implement, 
the  particles  of  dirt  which  may  fall  into  or  upon  the  cut  sur- 
face, or  from  the  ducts  of  the  glands  of  the  skin  itself.  It  may 
happen  that  the  fresh  tissues  thus  exposed  are  infected  with 
one,  or,  with  several  species  of  bacteria.  It  may  be  that  one 
or  more  of  these  species  may  be  destroyed  by  the  living  juices 
of  the  body  or  by  the  leucocytes,  or,  again  it  is  possible  that, 
from  their  .saprophytic  nature,  they  may  not  be  able  to  mul- 
tiph^  in  this  new  environment  ;  in  either  case  the  infection  is  of 
no  significance  and  clinically  would  not  be  recognized.  It  may 
happen  that  only  one  species  of  the  infecting  bacteria  multiplies 
and  produces  the  morbid  changes.  This  would  be  a  single  in- 
fection. If,  however,  two  or  more  species  co-operate  in  the  pro- 
duction of  the  lesions,  it  is  called  a  mixed  infection.  This  term 
is  often  used  to  designate  the  condition  where  one  species  may 
be  responsible  for  the  tissue  changes  although  other  bacteria 
are  present  but  in  an  accidental  or  passive  way  (§  4). 

(4)  Through  the  generative  organs.  Infection  of  there- 
productive  organs  takes  place  in  certain  instances  where  they 
are  the  seat  of  the  disease.  This  is  especialh'  true  in  case  of 
nialadie  du  coit. 

(5)  T/irough  the  agejier  0/  insects.  Some  insects  carry 
the  virus  of  certain  diseases  from  the  infected  and  introduce  it 
into  the  susceptible  individuals.  Thus  the  mosquito  carries 
the  Plasmodium  of  human  malaria,  the  cattle  tick  the  piroplasma 
of  Texas  cattle  fever  and  flies  are  often  the  introducers  of 
pathogenic  bacteria,  such  as  those  of  anthrax  (§  76). 

(6)  Transmission  0/  the  virus  from  the  parent  to  thefoettis. 
Occasionally  the  young  of  diseased   parents  are  born  infected 


5  WOUND    INFECTION 

with  the  disease  with  which  one  or  both  of  its  parents  were 
suffering.  In  these  cases  the  specific  bacteria  were  transmitted 
either  from  the  sire  at  the  time  of  coition,  or  later  to  the 
foetus  in  the  uterus  from  the  dam.  It  is  important  not  to 
confuse  these  rare  cases  with  those  in  which  the  offspring  are 
born  uninfected  but  subsequently  contract  the  disease.  Many 
of  the  so-called  hereditary  diseases  are  the  result  of  post  natal 
infection. 

§4.  Wound  infection.  Wound  infections  are  the  direct 
results  of  the  entrance  of  certain  microorganisms  into  trau- 
matisms and  operative  incisions.  They  fall  very  naturally 
into  two  classes  namely,  (i)  those  producing  acute  or  more 
chronic  inflammatory  processes  usually  leading  to  suppuration 
and  finally  healing  by  granulation,  and  (2)  iniections  which 
may  in  the  beginning  appear  like  the  first  or,  cause  so  little 
disturbance  as  to  be  unnoticed  at  the  time,  but  sooner  or  later 
result  in  a  local  or  remotely  situated  lesion  or  lesions.  Fre- 
quently these  are  recognized  as  distinct  diseases  although 
in  some  cases,  such  as  scirrhous  cord,  the  origin  is  easily 
traced  to  an  operation  where  infection  was  possible.  In  this 
second  group  of  wound  infections  there  are  in  addition  to  the 
scirrhous  cord  or  botryomycosis,  infectious  cellulitis  of  cattle 
and  sheep  and  still  other  disorders  which  may  not  seem  to  be 
dependent  upon  wound  infection  but  which  the  results  of  re- 
cent investigations  suggest  as  their  primary  cause.  These  af- 
fections will  be  treated  separately  in  subsequent  paragraphs 
but  their  relation  to  wound  infection  renders  them  worthy  of 
note  in  this  connection. 

A  third  class  should  be  mentioned,  namely,  those  specific 
diseases  such  as  tetanus  and  symptomatic  anthrax  where  the 
virus  is  supposed  always  to  be  introduced  through  a  wound 
either  in  the  skin  or  mucous  membranes. 

§  5.  Bacteria  causing  wound  infection.  A  large  num- 
ber of  species  of  bacteria  and  a  few  fungi  are  included  among 
the  organisms  which  are  known  to  produce  wound  infections 
in  animals.  Usually,  however,  the  forms  encountered  are 
micrococci,  especially  those  belonging  to  the  staphylococcus 
group,  streptococci,  a  few  bacilli,  especially  those  belonging  to 


BOTRYOMYCOSIS  7 

the  colon  group,  and  a  few  species  of  the  genus  pseudomonas 
Fungi  and  protozoa  are  rarely  found  in  wound  infection  le- 
sions. Many  of  the  specific  pathogenic  bacteria  may  be  intro- 
duced through  wounds  (§  3).  As  a  rule,  it  seems  to  be  true 
that  in  the  domesticated  animals  as  in  man  the  pyogenic 
bacteria  are  the  most  common  and  important  wound  infecting 
microorganisms.  In  open  wounds  these  are,  of  course,  asso- 
ciated with  a  very  large  number  of  ordinary  saprophytic  bac- 
teria. Frequently  in  closed  lesions  nonpathogenic  organisms 
are  present  in  addition  to  the  seemingly  causative  factors.  It 
is  worthy  of  note,  that  it  appears  to  be  impossible  to  predict 
from  the  general  character  of  the  lesions,  the  kind  of  bacteria 
which  are  producing  them  except  it  be  in  case  of  certain  spe- 
cific infections  like  tuberculosis  or  actinomycosis. 

^^  6.  Lesions  presumably  of  wound  infection  origin 
that  are  recognized  as  distinct  maladies.  It  has  already 
been  stated  that  the  lesions  following  wound  infections  may  be 
brought  about  by  a  variety  of  bacteria  and  also  that  certain  of 
these  diseased  processes  are  som.etimes  recognized  as  distinct 
maladies.  There  are  a  number  of  affections  which  belong  to 
this  class.  From  some  of  these,  such  as  botrj'omycosis,  a  sup- 
posedly specific  organism  has  been  isolated  and  described.  A 
number  of  workers,  however,  have  found  that  other  bacteria 
may  produce  apparently  the  same  morbid  conditions.  The  more 
important  of  the  affections  which  seem  to  be  directly  traceable 
to  wound  infection  will  be  briefly  described  in  the  light  of  re- 
cent investigations.  It  should  be  stated,  however,  that  the 
amount  of  work  that  has  been  done  on  these  subjects  is  not 
sufficient  to  render  the  resitlts  in  any-  way  conclusive,  but 
rather  to  suggest  the  lines  along  which  valuable  and  conclusive 
findings  may  be  expected  in  the  future. 

§  7.  Botryomycosis.  This  name  has  been  given  to  a 
variety  of  lesions  found  more  commonly  in  the  horse  but  occur- 
ring also  in  cattle,  swine  and  other  animals.  The  thickened 
spermatic  cord  (scirrhous  cord)  which  sometimes  follows  cas- 
tration is  the  most  common  form  of  this  disease.  Practitioners 
often  designate  as  botr3'omycosis  certain  closed  abscesses  occur- 
ring in  the  subcutaneous  or  intermuscular   tissue.     Abscesses 


8  BOTRYOMYCOSIS 

and  nodules  found  in  the  internal  organs  have  been  included 
under  this  caption.  Several  investigators  have  isolated  from 
these  lesions  a  species  of  microorganism  which  appeared  to 
stand  in  a  causative  relation  to  them.  It  was  first  described  as 
Zoogloea  pulmonis  equi,  in  1870,  by  Bollinger,  who  found  it  in 
the  nodules  in  the  lungs  of  a  horse.  More  recently  he  has  re- 
named it  Botryococcus  ascofor'inans.  Rivolta  designated  it  Dis- 
comyces  equi.  Rabe  proposed  the  name  Micrococcus  botryogenes 
and  Johne  has  "called  it  M.  ascoformaus.  The  results  of  other 
investigators  throw  some  doubt  upon  the  specific  nature  of 
these  lesions.  Kitt,  Hell,  dejong.  Gay  and  others  have  found 
in  them  micrococci  which  do  not  differ  from  M.  pyogenes  aureus. 
The  writer  has  failed  to  find  M.  ascofornians  but  has  isolated 
in  its  .stead  pyogenic  micrococci  and  streptococci.  In  one  very 
interesting  case  of  thickened  cord,  the  writer  found  masses  of  a 
fungus  resembling  that  of  actinomycosis  within  the  pockets  of 
spong}'  tissue  sprinkled  throughout  the  thickened  fibrous  cord. 
Bacteria  were  not  found  in  this  case.  In  the  closed  abscesses 
in  the  connective  tissue  pyogenic  bacteria  have  been  found,  ex- 
cepting in  certain  cases  of  long  standing  where  the  cultures 
gave  negative  results.  Investigations  which  have  been  made 
into  the  bacterial  flora  of  the  skin  of  the  horse  show  that 
P3^ogenic  bacteria  are  frequently  present  in  the  deeper  layers 
of  the  epidermis,  in  ducts  of  glands  and  about  the  hair  shafts. 
With  the  possibility  of  infection  from  the  integument  plus  all 
the  other  chances  of  having  members  of  this  and  other  groups 
of  bacteria  introduced  into  the  body  there  seems  to  be  abundant 
opportunity  for  infection  by  a  variet}^  of  species.  The  evi- 
dence at  hand  points  to  the  conclusion  that  botryomycosis  is 
the  result  of  wound  infection,  and  that  several  species  of  micro- 
organisms are  capable  of  producing  it. 

§  8.  Omphalophlebitis.  This  affection  which  is  com- 
monly called  navel-ill,  consists  of  suppurative  lesions  in  j'oung 
animals  caused  by  pyogenic  bacteria.  In  the  horse  they  are 
most  often  localized  in  the  joints  of  the  limbs.  In  certain  other 
species  the  lesions  are  quite  as  likely  to  be  situated  elsewhere 
in  the  body.  In  some  cases  the  morbid  changes  are  restricted 
to  subcutaneous  and  intermuscular  suppurative  cellulitis. 


OMPHALOPHLEBITIS  9 

The  infection  takes  place  in  the  umbihcus.  As  the  cord 
is  severed  in  the  field  or  stable  many  species  of  bacteria  may 
gain  access  to  the  end  of  the  exposed,  and  freshly  severed 
cord.  In  the  colt,  a  streptococcus  seems  to  be  the  most  com- 
mon species  of  bacteria  capable  of  producing  the  joint  ab- 
scesses. In  the  lamb,  a  variety  of  the  colon  bacillus  has  been 
associated  apparently  as  the  etiological  factor  with  the  subcu- 
taneous cellulitis.  The  lesions  resulting  from  naval  infection 
illustrates  in  a  most  excellent  manner  the  extent  to  which 
certain  pyogenic  bacteria  gaining  access  to  the  body  may 
extend  by  metastasis  to  places  remote  from  their  entrance  and 
produce  diseased  foci. 

In  cases  of  navel-ill,  the  umbilical  \ein  contains  a  large 
number  of  bacteria.  The  writer  has  found  that  in  colts  very 
few  if  an\'  of  the  bacteria  (streptococci)  producing  the  joint 
lesions  could  be  found  in  the  parenchymatous  organs.  Occasion- 
ally one  or  two  of  many  tubes  of  media  inoculated  from  the 
liver  would  develop  into  cultures  of  the  infecting  organism. 
In  this  disease,  where  many  species  of  bacteria  come  into  com- 
petition, one  is  impressed  with  the  fact  that  seemingly  very 
few  of  the  ordinary  bacteria  are  capable  of  gaining  an  entrance 
into  the  circulation  or,  at  least,  are  possessed  of  vital  powers 
sufficient  to  resist  the  destructive  forces  of  the  living  animal 
body.  A  brief  description  of  a  case  with  the  bacterial  findings 
will  illustrate  this  point.  The  case  referred  to  was  from  Dr. 
Williams'  clinic. 

A  colt,  about  three  weeks  old.  It  was  in  good  condition  and  seemed 
to  be  perfectly  well  excepting  for  the  diseased  joints.  It  was  killed  for 
examination.  The  umbilical  vein,  from  the  umbilicus  to  the  liver,  was 
distended  with  blood,  pus  cells  and  bacteria.  All  of  the  internal  organs 
appeared  to  be  normal.  In  both  knee  joints  and  in  one  hock  joint,  there 
was  extensive  suppuration.  A  bacteriological  examination  showed  the 
umbilical  vein  to  contain  many  species  of  bacteria,  among  which  may  be 
mentioned  B.  coli  coinmiiuis,  Micrococcus  pyogenes  aureus  and  a  strepto- 
coccus. One  of  several  tubes  of  media  inoculated  from  the  liver  devel- 
oped the  streptococcus,  the  others  remained  clear.  All  media  inoculated 
from  the  heart  blood,  spleen,  kidney  and  glands  remained  sterile.  All 
of  the  media  inoculated  with  the  pus  from  the  diseased  joints  gave  pure 
cultures  of  the  streptococcus. 


lO  WHITE    SCOURS    IN    CALVES 

§  9.  White  scours  or  diarrhoea  in  calves.  This  is  a 
disease  affecting  calves  from  a  few  hours  to  as  many  daj's 
old,  with  a  mortalitj-  ranging  from  50  to  90  per  cent.  The  in- 
vestigations which  have  been  made  in  this  country,  especially 
those  at  the  New  York  State  Veterinary  College,  have  sug- 
gested that  it  is  due  to  certain  forms  of  the  colon  bacillus.  In 
these  investigations  characteristic  lesions  were  not  found,  the 
calves  presenting  simply  a  general  anaemic  condition. 

Recently,  Nocard  has  reported  the  results  of  his  investiga- 
tion of  apparently  a  similar  disease  of  calves  in  Ireland.  He 
found  that  they  usuall}'  die  during  the  first  week.  In  the  more 
chronic  cases,  lung  lesions  were  found.  His  inquiries  tend  to 
show  that  this  is  primarily  due  to  a  wound  infection.  He 
states  in  his  report  concerning  the  nature  of  this  disease  that 
it  usuall}'  lasts  from  3  to  6  days  and  is  characterized  by  an  in- 
tense intestinal  discharge.  The  discharges  are  always  of  the 
nature  of  a  diarrhoea,  white,  and  frothy.  The  calves  lose 
flesh  rapidly,  their  flanks  are  hollow,  abdomen  retracted,  back 
arched,  eyes  sunken,  hair  dull  and  staring  ;  they  make  violent 
expulsive  efforts,  the  nose  is  hot  and  dry  with  slight  discharge 
of  mucus,  and  the  temperature  is  elevated. 

In  other  cases,  but  not  so  commonly,  the  symptoms  are  less 
severe  and  recovery  seems  to  take  place  but  most  of  the  calves 
die  several  weeks  later  with  pulmonary  lesions. 

Nocard  also  states  that  it  is  not  rare  to  see,  in  the  cases, 
the  discharges  mixed  with  blood  in  various  quantities.  In 
more  chronic  forms  it  is  not  rare  to  observe  acute,  multiple  and 
very  painful  arthritis. 

The  lesions  found  at  the  autopsy  vary  according  to  the 
course  of  the  disease.  Usually  the  umbilicus  is  large  and  the 
umbilical  blood  vessels  have  indurated  walls,  and  contain 
blood  clots  which  may  be  soft  and  purulent.  Blood}^  extrav- 
asations are  observed,  sometimes  very  extensive,  along  the 
umbilical  vessels  and  the  urachus,  extending  sometimes  to  the 
posterior  third  of  the  bladder. 

In  rapidly  progressing  cases,  lesions  of  true  hemorrhagic 
septicaemia  are  found.  All  the  organs  are  congested  :  their 
surface  is  covered    with    petechiae,  ecchymoses  or  sub-serous 


WHITE    SCOURS    IN    CALVES  II 

blood  infiltrations  ;  the  capillary  network  of  the  peritoneum, 
the  omentum,  the  pleura  and  the  pericardium  is  very  much 
injected. 

Nocard  describes  the  lungs  and  articular  lesions  as  follows  : 

"The  lungs  are  rarely  entirely  healthy  ;  most  often  they 
present  here  and  there  little  diffuse  centers  of  catarrhal  pneu- 
monia, nodular  broncho-pneumonia  or  only  of  atelectasis.  The 
lesions  are  much  more  constant,  extensive  and  dense  when  the 
animals  have  resisted  longer  ;  they  represent  then  the  transi- 
tion between  the  simple  atelectasis  of  the  beginning  and  the 
suppurative  lesion  of  lung  disease." 

"Articular  lesions,  when  they  exist,  are  very  interesting. 
The  periarticular  tissues  are  infiltrated  with  5'ellowish  and 
somewhat  gelatinous  liquid  ;  the  .synovial  serous  membrane  is 
covered  with  a  rich  vascular  injection,  which  seems  to  extend 
to  the  borders  of  the  cartilages  of  the  articular  surfaces  ;  the 
culs-de-sac  of  the  synovials  are  distended  by  a  great  quantity 
of  thick  and  limpid  synovia,  strongly  yellow  or  reddish  in 
color,  and  in  which  more  or  less  dense  and  abundant  clots  of 
fibrinous  exudate  are  floating.  When  the  lesion  is  older,  in- 
stead of  synovia,  there  are  thick,  dense,  and  firm  fibrinous 
exudates,  which  fill  the  culs-de-sac  of  the  serous  membrane 
and  are  infiltrated  between  the  articular  surfaces.  In  these 
cases  the  lesion  resembles  exactly  those  of  peripneumonic 
arthritis  of  suckling  calves." 

He  found  a  microorganism  (pasteurellose)  in  the  organs 
and  blood  of  the  calves,  with  which  he  was  able  to  produce 
the  disease.  After  convincing  himself  that  he  had  found  the 
cause  ,he  sought  for  the  source  of  infection  which  he  found  in 
the  umbilicus.  He  advances  three  suppo.sitions  concerning  the 
time  and  mode  of  entrance  :  i.  intra-uterine,  2.  vaginal,  3.  after 
delivery  when  the  calf  drops  on  the  ground  or  floor  and  when 
the  ruptured  cord  comes  in  contact  with  the  fecal  matter  or  dust 
of  the  stable.  The  latter  he  beliefs  to  be  the  correct  method. 
His  conclusion  concerning  infection  after  delivery  may  be 
summarized  in  the  following  observation  which  he  makes  : 

"We  have  witnessed  in  a  well  kept  farm  a  case  of  labor  in 
a  cow.     She  was  in  an  ordinary  barn.     Nothing  had  been  pre- 


12  WHITE    SCOURS    IN    CALVES 

pared  to  receive  the  new-born.  The  calf  was  dropped  on  a 
bedding  soiled  with  feces  ;  he  only  fell  back  a  little,  and  there 
during  15  or  20  minutes,  we  watched  him  making  his  efforts  to 
get  up,  falling  back  here  and  there  to  the  right  and  to  the  left 
or  on  his  belly,  dragging  the  stump  of  his  cord  on  the  ground, 
in  the  urine,  or  even  in  the  fecal  matter.  It  was  only  after  the 
mother  had  well  licked  her  little  one,  well  covered  with  salt, 
that  the  cord  was  ligated.  lam  not  sure  that  the  umbilicus 
was  cleaned. 

White  scours  is  ordinarily  the  result  of  umbilical  infection 
which  takes  place  at  the  time  of  delivery,  by  the  way  of  the 
wound  made  by  the  rupture  of  the  cord." 

He  states  that  this  trouble  can  be  prevented  if  the  person 
in  charge  of  the  animals  at  the  time  of  their  delivery  takes 
certain  precautions  to  prevent  infection.* 

This  disease  described  by  Nocard  does  not  seem  to  differ 
in  many  respects  from  the   diarrhoea   in    young   calves  in  this 


*"i.  Cows  ready  to  calve  should  be  provided  with  dry  and  clean 
bedding  until  after  the  birth  of  the  calf. 

2.  As  soon  as  labor  sets  in  the  vulva,  anus  and  perineum  should  be 
cleaned  with  a  tepid  solution  of  lysol  in  rain  water  ;  twenty  grammes  of 
lysol  for  each  litre  of  water.  The  vagina  should  also  be  cleaned  by  in- 
jecting with  a  large  syringe  a  great  quantity  of  the  same  tepid  solution. 

3.  The  calf  should  be  received  on  a  clean  cloth  or  at  least  upon  a 
thick  fresh  bedding  not  soiled  by  urine  or  feces. 

4.  The  cord  should  be  tied  immediately  after  birth  with  a  ligature 
previously  kept  in  a  lysol  solution,  and  the  cord  amputated  below  the 
ligature. 

5.  The  stump  of  the  cord  and  the  umbilicus  should  be  washed  with 
the  following  solution  : 

Rain  water,  i  litre. 

Crystals  of  iodine,  2  grammes. 

Iodide  of  potassium,         4  grammes. 

6.  The  disinfection  of  the  umbilicus  and  the  cord  should  be  followed 
by  coating  the  umbilicus  with  a  solution  consisting  of 

Methylic  alcohol,  i  litre. 

Crystals  of  iodine,  2  grammes. 

7.  The  operation  should  be  closed,  after  the  alcohol  has  evaporated, 
by  coating  the  cord  and  umbilicus  with  a  thick  layer  of  iodine  collodion 
(i  percent)  applied  with  a  brush.  Once  the  collodion  is  dried,  the  calf 
may  be  left  to  the  care  of  its  mother." 


INFECTIOUS    CELLULITIS  1 3 

country.  Ward  and  Fisher  are  making  careful  tests  of  his 
method  with  quite  satisfactory  results.  In  our  cases  the  lung 
complications  did  not  occur.  The  important  finding  of  Nocard 
should  stimulate  further  investigation  into  this  mo.st  important 
trouble  in  this  country.  As  the  remedy  which  he  recom- 
mends and  which  has  given  good  results  is  simpl}-  one  to 
prevent  infection  of  the  ruptured  cord,  the  conclusion  tends  to 
the  wound  infection  origin  of  tliis  disease. 

§  lo.  Infectious  suppurative  cellulitis.  Cattle  and 
sheep  suffer  from  more  or  less  extensive  iuflammator}'  condi- 
tions of  the  subcutaneous  tissues  especially  of  the  lower  ex- 
tremities. Frequently  the  morbid  process  extends  beneath  the 
hoof  causing  it  to  slough  or  to  undergo  resulting  disintegration 
changes.  When  this  condition  exists,  the  affection  is  usually 
called  "foot  rot."  If  the  inflammatory  process  attacks  the  skin 
also,  the  condition  is  often  designated  erysipelas.  If  it  becomes 
circumscribed,  resulting  in  a  local  suppuration,  an  abscess  or  an 
ulcer  is  the  result.  The  investigations  which  have  been  made 
concerning  the  cause  of  these  lesions  point  to  the  conclusion 
that  they  result  from  an  infection,  probabl}-  through  some 
slight  abrasion  of  the  skin.  Thus  far,  the  results  show  strep- 
tococci* to  be  the  etiological  factors  in  the  majority  of  these 
cases.  It  frequently  happens  that  a  number  of  animals  sub- 
jected to  the  same  conditions  are  attacked  at  the  same  time, 
giving  rise  to  a  condition  resembling  an  epizootic.  In  cattle, 
cases  studied  by  the  writer, — the  lesions  were,  within  certain 
limits,  uniform  in  all  of  the  affected  animals.  Usually  but 
one  foot  or  leg  was  attacked,  although  there  were  numerous 
exceptions.  The  first  symptom  noticed  was  a  swelling,  which 
usually'  appeared  in  the  lower  part  of  the  leg,  most  often  in  the 
pastern.  In  some  animals  the  swelling  was  restricted  to  a  small 
area,  but  often  it  extended  up  the  leg  to  and  even  above  the 
knee  or  the  hock  joint.  There  was  evidence  of  pain.  As  the  in- 
flammatory process  continued,  the  subcutaneous  tissue  became 


*Lucet  has  reported  the  results  of  bacteriologic  examinations  of  fifty- 
two  abscesses  in  cattle.  From  nine  of  these  streptococci  were  obtained 
in  pure  culture,  and  in  ten  cases  they  were  associated  with  other  bacteria. 
— Annates  de  V Institut  Pasteur.      Vol.  VII {iSgj)  p.  ^24. 


14  INFECTIOUS    CELLULITIS 

indurated,  the  skin  thick  and  dr}',  and  later  it  would  crack, 
usually  but  not  always,  below  the  dew  claws,  and  a  thick  creamy 
pus  would  be  discharged.  After  discharging,  the  swelling 
subsided  and  the  normal  condition  was  rapidly  restored.  The 
time  necessary  for  the  suppurative  process  and  recovery  to 
take  place  varied  in  different  animals,  but  as  a  rule  from  ten 
to  fifteen  days  were  required.  The  exceptions  were  largely  in 
those  cases  where  the  inflammator}-  process  extended  down  to 
the  coronary  cushion.  In  these  there  was  more  or  less  slough- 
ing of  the  hoof.  It  is  in  these  cases  that  the  disea.se  is  most 
serious. 

In  the  so-called   foot-rot  of  sheep,  we   have,  in  the  cases 
which  have  come  to  our  notice,  conditions  similar  to  those  found 
in  the  cattle  which  were  suffering   from  suppurative  cellulitis. 
It  may  be  of  interest  to  cite   a   specific  case  with    the  result  of 
the  bacteriological  examinations. 

May,  1899,  two  sheep  that  were  suffering  from  so-called 
foot- rot  were  brought  to  Dr.  Law's  clinic.  They  came  from  a 
large  flock  in  which  forty  or  more  animals  were  reported  to  be 
similarl}^  affected. 

No.  I.  An  adult  female  in  very  poor  condition.  All  four  feet  and 
legs  were  affected  and  the  nails  on  one  foot  were  quite  loose.  There  was 
a  purulent  discharge  from  openings  either  between  the  claws  or  in  the 
skin  just  above  the  hoof.  The  microscopic  examination  of  the  pus  from 
this  opening  showed  a  number  of  bacteria  but  streptococci  were  especially 
numerous.  They  were  not  isolated  in  pure  culture.  The  left  knee  was 
badly  swollen  and  from  the  lower  side  of  the  swelling  there  was  a  dis- 
charge of  thin  purulent  substance  which  contained  streptococci  in  large 
numbers.  A  few  other  bacteria,  mostly  micrococci,  were  associated  with 
them. 

No.  2.  An  adult  female,  black,  emaciated,  but  in  much  better  flesh 
than  No.  i.  The  two  fore  feet  and  the  left  hind  one  were  affected.  The 
hind  foot  and  the  right  fore  one  were  discharging.  The  left  fore  foot 
was  badly  swollen  above  the  hoof  but  the  swelling  did  not  extend  high 
up  the  leg.  Fluctuation  was  marked.  The  skin  was  shaved,  washed, 
disinfected  and  the  abscess  opened.  A  thick  creamy  pus  was  expressed. 
From  this  a  number  of  tubes  of  media  were  inoculated  and  in  each  a 
streptococcus  developed  in  pure  culture.  The  pus  from  the  discharging 
feet  contained  a  streptococcus  with  other  bacteria.  The  feet  were  treated 
locally  with  disinfectants  by  Dr.  Law.     In   recovering  there  was  consid- 


FISTULOUS    WITHERS    AND    POLL-EVIL  15 

erable  thickening  of  the  interdigital  tissue.     In  this  case  the  suppuration 
had  not  extended  under  the  nails. 

§  II.     Fistulous  withers  and  poll-evil.     Recent  inves- 
tigations indicate  that   these   very  common    and    troublesome 
local  diseased   conditions  are  either  directly  or  indirectly  the 
result  of  bacterial  invasion.     This  conclusion    is    tentatively 
drawn  from  the  fact  that  the  bacteriological  examinations  made 
from  the  pus  and  from  recent  lesions  in  these  affections  invari- 
ably reveal  the  presence  of  streptococci  or  micrococci,  or  both. 
Gay  found  a  streptococcus  in  each  of  seven  cases  of  common 
fistulous  withers  and  in  two  cases  of  poll-evil.     It  was  invariably 
associated    with    a    micrococcus.      He    found  in   five  cases  of 
deep  seated  shoulder  abscesses  M.  pyogeiies  aureus  only.     It  is 
instructive  to  note,  that  bacteria  closely  resembling  this   or- 
ganism has  frequently  been   found   in  the  deeper  layers  of  the 
skin.     The  mechanical   injuries  commonly   attributed    as  the 
primary  cause  consist  usually  of  little  more  than  skin  irritation 
from  ill  fitting  harnesses,  saddles  or  from  blows.     While  these 
are  mechanically  not  extensive,  they  are   sufficient  to  liberate 
into  the  juices  of  the  subjacent  tissues  the  bacteria  deeply  seated 
in  the  integument.     The  inflammatory  process  leading  to  sup- 
puration, the  formation  of  fistulse,  the  new  formation  of  fibrous 
tissue  in  the  affected  parts,  and  even  the  bone  necrosis  occa- 
sionally seen  are  all  possible  and  rational  results  of  the  activi- 
ties of  the  pyogenic  bacteria  found   in  the  lesions.     There  is 
nothing  in  their  character  to   suggest  causative  agencies  other 
than  microorganisms.     The  changes  involved  in  the  inflamma- 
tory process,  the  deposition  of  fibrous  tissue,  and  the  abscess 
formation  all  belong  more  proper]  \-  to  general  pathology  and 
need  not  be  discussed   here.      These  affections  are  mentioned 
in  this  connection  simply  because  the  accumulating  evidence 
tends  to  strengthen  the  working  hypothesis  that  they  are   the 
result  of  bacterial  invasion. 

§12.  Infectious  Mastitis.  Cattle  suffer  frequently  from 
an  acute  inflammation  of  the  udder  as  the  result  apparently  of 
an  invasion  by  a  number  of  bacteria.  The  results  of  the  inves- 
tigation of  this  affection  thus  far  reported  suggest  that  the 
form  which  is  transmitted   from  animal  to  animal  is  caused  by 


1 6  MASTITIS 


,,/•••,  a  Streptococcus  (Fig.  I ).     It  is, 

Ci^o*^^**"*         »M  however,  difficult  to  distinguish 


.    ^^^     ^.,^Vo       /# 


■) 


between  this  affection  and  those 


•     -«         —■     •— ••.  *      •'^     .       caused  bv  certain  other  bacteria. 


r,  ^   ^       ^ ''o  2       I^  seems  likely  that  many  cases 

are  primarily  brought  about  by 

mechanical  injuries  which  ren- 

.    ^^    ^         -         der  possible  the  entrance  into 

tl     •  \    ^  ®  of  the  skin  or  of  the  milk  ducts. 

••'  Other  ca.ses  may  be  due  to  in- 

FiG.  I.     Streptococcus  from  a     faction  through  the  teat  of  bac- 

case  of  infectious  mastitis.  «.     •  u^        c  i      ■  i 

-^     -^  teria  capable  of  producing,  by 

means  of  their  metabolic  products,  the  inflammatory  condition 
without  a  distinct  injury  to  the  mucous  membrane.  The  for- 
mer view  that  there  was  a  sphincter  muscle  near  the  base  of 
the  teat  which  closed  the  duct  sufficiently  to  prevent  the  en- 
trance of  bacteria  to  the  secreting  portions  of  the  gland  was  not 
well  founded  upon  anatomical  facts  (Fig.  2). 

The  acute  and  more  chronic  inflammator}'  affections  of  the 
udder  fall  very  naturally  into  two  groups,  namely, (i)  those  in 
which  the  parenchyma  is  most  affected  and  (2)  those  in  which  the 
stroma  or  fibrous  tissue  is  involved.  The  form  of  mastitis  more 
frequently  encountered  as  an  infectious  (transmissible)  disease  is 
characterized  by  very  marked  changes  in  the  milk  accompanied 
by  the  usual  symptoms  of  parench^miatous  inflammation  of 
the  gland  itself.  The  discharge  from  the  udder  usually  con- 
tains flaky  masses  held  in  suspension  in  the  clear  or  perhaps 
cloudy  .serum.  The  color  varies,  and  occasionally  the  mass  is 
blood-stained.  The  microscopic  examination  shows  the  pres- 
ence of  agglutinated  fat  globules,  pus  cells,  and  often  red  blood 
corpu.scles. 

A  number  of  bacteria*  considered  of  more  or  less  etiological 


♦Among  the  bacteria  which  have  been  found  in  udder  trouble  and 
described  as  the  possible  or  perhaps  the  more  probable  cause  the  follow- 
ing species  may  be  mentioned  : 

Bacterium  phlegniasics  uteris.  Streptococcus  agalacticr  coyitagiosce. 
Staphylococcus  mastitidis,  Galactococcus  versicolor,  G.fulvus,  G.  albus. 


SECTION    OF   UDDER 


17 


Fig.  2.  Section  of  cow's  udder  through  one  teat  {a)' cistern,  (b) 
larger  milk  ducts,  [c]  secreting por'tion  of  niainniary gland.  2,  drawing 
of  secreting  portion  of  gland  enlarged. 


l8  MASTITIS 

value  have  been  found  associated  with  lesions  of  doubtful  spe- 
cific origin.  The  results  of  Kitt,  Nocard,  Mollereau,  Guille- 
beau,  Zschokke,  Bang  and  still  others  in  which  a  Bacterium,  a 
Micrococcus,  a  Staphylococcus,  and  a  Streptococcus  have  been 
found  and  reported  as  standing  in  a  causal  relation  to  the 
trouble,  indicate  that  a  variet}'  of  microorganisms  are  active  in 
producing  those  affections  which  are  frequently  grouped  with- 
out distinction  as  infectious  mastitis.  The  review  of  much  of 
the  literature  on  this  subject,  shows  that  a  number  of  cases  re- 
ported as  infectious  were  isolated  or  sporadic  ones,  /.  <?. ,  they 
were  in  dairies  where  the  disease  did  not  spread  to  other  ani- 
mals. While  these  may  be  truly  infectious  in  their  nature  they 
should  be  differentiated  from  the  rapidly  spreading  phlegmons 
which  are  easily  recognized  as  infectious  (contagious). 

If  we  take  into  account  the  variety  of  anatomical  changes 
which  have  been  described  in  the  various  udder  affections,  we 
can  reasonably  admit  that  different  agencies  may  have  been  in- 
strumental in  their  production.  The  various  species  of  bacteria 
which  have  been  isolated  from  the  udder  lesions  may  very 
likely  have  been  of  etiological  importance  in  their  respective 
cases. 

Already  the  facts  have  been  pointed  out,  that  the  udder  is 
normally  more  or  less  extensively  invaded  with  bacteria  and 
that  certain  species  of  bacteria  seem  to  persist  in  the  milk 
ducts  of  the  glands  when  once  they  become  lodged  there.  If 
these  results  apply  to  cows  generally  as  rigidly  as  they  did  to 
those  examined,  an  explanation  for  the  presence  of  a  variety 
of  bacteria  in  the  affected  udders  is  not  difficult  to  find. 
Whether  these  particular  organisms,  under  certain  conditions, 
would  become  primarily  responsible  for  udder  disease  is  not 
known.  The  evidence  suggests  that  a  number  of  the  bacteria, 
heretofore  described  as  the  cause  of  mammitis,  were  in  the 
affected  glands  by  virtue  of  their  presence  in  the  normal  udder. 
Concerning  these  points  additional  investigations  are  much 
needed. 

The  writer  has  examined  the  secretions  from  two  quite 
serious  outbreaks  of  mastitis.  In  the  first,  the  milk  was  drawn 
in  sterile  bottles  after  the  udders  and  the  hands  of  the  milker 


A   SPECIFIC   INFECTIOUS   DISEASE  1 9 

had  been  thoroughly  washed  in  a  i  to  looo  solution  of  corrosive 
sublimate.  In  all,  there  were  eight  samples  of  milk  taken 
from  as  many  different  cows.  In  six  of  the  eight  specimens 
streptococci  appeared  in  pure  culture.  In  the  other  two  cases 
micrococci  were  associated  with  the  streptococcus.  In  the 
second  outbreak,  the  milk  from  four  diseased  udders  was  drawn 
with  aseptic  precautions  directly  into  tubes  containing  slant 
agar  and  promptly  sent  to  the  laboratory  where  it  was  carefully 
examined.  From  two  cases  pure  cultures  of  streptococci  were 
obtained  while  those  from  the  others  were  impure.  The  strep- 
tococci obtained  from  the  twelve  cases  appeared  to  be  identical 
and  the  clinical  aspect  of  the  disease  in  the  different  animals 
was  the  same. 

In  a  dairy  that  was  under  close  ob.servation  by  Ward,  one 
cow  was  found  to  be  troubled  in  one  quarter  of  the  udder  with 
an  inflammatory  process  which  produced  thickened  masses  in 
the  blood-stained  milk.  From  this  milk  a  streptococcus  was 
isolated  in  pure  culture.  It  could  not  be  differentiated  from 
the  one  isolated  from  the  cows  in  the  outbreaks  mentioned. 
Another  cow  in  this  herd  was  found  to  have  her  udder  per- 
manently infected  with  a  streptococcus.  Another  animal  in  the 
same  dairy  suffers  repeatedly  from  acute  streptococcus  mastitis. 

There  are  a  large  number  of  morbid  conditions  more  or 
less  frequently  encountered  in  domesticated  animals  which 
seem  to  be  due  to  infection  of  some  kind  but  which  are  not 
demonstrated  to  be  of  such  an  origin.  These  will  continue  to 
be  attributed  b}'  some  to  infection  and  by  others  to  various  gen- 
eral causes  until  the  truth  concerning  their  etiology  is  revealed. 

^  13.  A  specific  infectious  disease.  A  specific  infec- 
tious disease  is  the  result  of  the  multiplication  within  the  animal 
body  of  a  single  species  of  microorganisms.  The  lesions  may 
be  localiztd  or  general  but  the  cause  producing  them  is  always 
the  same.  Thus  Bacterium  aiithracis  will  produce  a  disease 
which  is  called  anthrax,  no  other  cause  can  produce  it  and  no 
matter  how  much  the  lesions  ma}-  var}-  in  different  individuals 
if  they  are  produced  by  this  species  of  bacteria  the  disease  is 
anthrax.  It  is  clear,  therefore,  that  there  is  no  hard  and  fast 
line  between  a  simple  (single)  wound  infection  and  a  recognized 


20  CHARACTERS    OF    AN    EPIZOOTIC    DISEASE 

infectious  or  epizootic  disease  except  in  the  nature  of  the  in- 
vading organism.  The  lesions  may  vary  and  usually  they  do 
especialh'  in  different  species  of  animals.  If  a  man  receives 
accidentally  a  cut  from  a  knife  with  which  he  is  making  a  post 
mortem  on  an  animal  dead  from  anthrax,  the  lesion  is  liable  to 
be  restricted  to  the  point  of  inoculation,  and  while  it  is  anthrax 
(malignant  pustule)  it  would  very  often  be  recognized  as  a 
simple  wound  infection.  If  this  accidental  inoculation  should 
occur  in  a  guinea  pig,  the  disease  would  not  be  recognized 
as  a  local  lesion  ;  but  the  animal  would  most  likely  die  of 
septicaemia  (§2). 

As  a  class,  the  lesions  known  clinically  as  wound  infections 
are  differentiated  from  the  specific  diseases  in  a  number  of  ways. 
The  bacteria  commonly  found  in  wound  infections  do  not  pro- 
duce the  epizootic  diseases,  although  there  are  notable  excep- 
tions. x-Ygain,  there  is  usually  a  difference  in  the  mode  of  in- 
fection. The  virus  of  the  epizootic  disease  is  ordinarily  intro- 
duced through  the  digestive  or  respiratory  tract  or  by  means 
of  insects,  while  in  wound  infection  the  virus  is  introduced,  as 
the  term  implies,  through  the  injured  integument  or  mucosa. 

§  14.  The  differential  characters  of  a  specific  infec- 
tious or  epizootic  disease.  It  is  very  important  not  to  mis- 
take for  an  infectious  disease  some  form  of  body  disturbance 
due  to  a  local  cause  or  condition.  Animals  often  suffer  from 
improper  food  and  the  conditions  of  life  under  which  they  are 
compelled  to  live.  It  frequently  happens  that  as  all  of  the 
animals  in  a  given  herd  are  subjected  to  like  conditions,  a 
number  of  them,  perhaps  all,  will  manifest  very  similar  symp- 
toms and  more  or  less  of  them  die.  Such  an  occurrence  often 
gives  rise  to  the  supposition  that  the  cause  of  death  is  some 
form  of  infectfon.  Deaths  from  such  causes  or  under  such 
conditions,  should  be  carefully  distinguished  from  an  epizootic. 
In  differentiating  a  non-infectious  disorder  from  a  specific  dis- 
ease, it  is  important  and  usually  sufficient  to  take  into  account 
the  appended  characteristics  of  an  infectious  disease. 

(i)  An  infectious  disease  is  caused  by  a  specific  agent. 
This  necessitates  as  the  first  requisite  an  exposure  to  and  an 
infection  with  the  specific  organism  or  etiological  factor. 


EPIZOOTIC    DISEASE  21 

(2)  The  infection  must  be  followed  by  a  certain  period  of 
incubation  before  the  development  of  symptoms.  This  is  the 
time  necessary  for  the  invading  microorganism  to  become  es- 
tablished in  the  body  and  to  bring  about  the  first  symptoms  of 
the  disease.  The  incubation  period  varies  in  different  diseases 
and  to  a  certain  degree  in  the  same  disease  according  to  the 
mode  of  infection  and  the  resistance  of  the  individual.  Usu- 
ally the  incubation  period  of  a  given  disease  is  practically  the 
same  for  all  individuals  of  the  same  species  when  subjected  to 
the  same  mode  of  infection.    Exceptions,  however,  are  not  rare. 

(3)  The  course  of  an  infectious  disease  is  usually  nearly 
the  same  in  animals  suffering  in  the  same  outbreak  especially 
when  they  were  infected  at  or  about  the  same  time.  It  is  more 
common  for  only  a  few  individuals  in  a  herd  to  be  infected  in 
the  beginning  and  from  these  first  cases  other  animals  con- 
tract the  disease.  In  many  epizootics,  the  disease  appears  in 
an  acute  form  in  the  first  animals  attacked  while  those  infected 
later  in  the  course  of  the  outbreak  suffer  from  a  chronic  form 
of  the  disease.  In  other  outbreaks,  the  first  cases  are  chronic 
in  nature  and  the  later  ones  acute. 

(4)  In  animals,  as  in  man,  most  of  the  infectious  diseases 
are  self  limiting,  but,  as  a  rule,  the  percentage  of  fatal  cases  is 
much  larger  among  animals  than  in  the  human  species.  The 
period  of  convalescence  is  not  so  well  marked  in  the  lower 
species  as  in  man.  It  frequently  happens  that  the  course  of 
the  disease  is  so  changed  that  an  acute  case  which  appears  to 
recover,  or  at  least  to  pass  into  the  stage  of  convalescence,  be- 
comes chronic  or  sub  chronic  in  nature  and  eventually  termin- 
ates in  death.  The  lateness  in  the  development  of  the  modified 
lesions  often  causes  the  nature  of  the  terminal  disease  to  be 
unrecognized. 

(5 )  Finally,  it  is  necessary  in  making  a  positive  diognosis 
to  find  the  specific  organism,  or  to  prove  the  transmissibility 
of  the  malady  from  the  sick  or  dead  to  healthy  animals.  The 
extent  of  the  spread  of  the  virus  of  the  disease,  through  the 
available  channels  for  its  dissemination,  will  also  aid  in  deter- 
mining the  infectious  or  non-infectious  nature  of  the  disease  in 
an  outbreak  among  animals. 


22  CAUSE    OF    VARIATIONS 

§  15.  Cause  for  the  variations  in  the  course  of  an  in- 
fectious disease.  It  is  a  recognized  fact  that  there  is  much 
variation  in  the  course  of  infectious  diseases  in  different  epizo- 
otics and  often  marked  individual  variations  occur  in  the  same 
outbreak.  In  explaining  this  interesting  phenomenon,  it  is 
important  to  take  into  account  the  question  of  individual  resist- 
ance or  immunity — partial  or  more  complete.  It  was  found  in 
case  of  certain  diseases  that  when  an  individual  is  partiallj'  im- 
munized and  then  infected  that  the  lesions  were  very  much 
modified.  The  teachings  of  a  specific  etiology  pointed  to  this 
phenomenon  as  a  result  of  certain  biological  or  vital  differences 
existing  either  in  the  parasite  or  in  the  host,  possibly  in  both. 
The  results  of  the  investigations  already  made  along  this  line, 
suggest  a  probable  explanation,  that  the  course  of  the  disease 
varies  on  the  one  side  with  the  resistance  of  the  host  and  on 
the  other  with  the  degree  of  virulence  of  the  infecting  micro- 
organism.    This  has  been  expressed  in  the  formula 

r 

in  which  d  ^=  the  disease,  v  =  the  virulence  of  the  infecting: 
organism,  and  r  =  the  resistance  of  the  host  or  the  individual 
attacked.  As  v  or  r  change  the  disease  is  modified.  For  ex- 
ample, rabbits  that  are  partially  immunized  against  swine 
plague  bacteria,  when  inoculated  with  a  virulent  culture  of  that 
organism,  will  live  for  several  days  and  perhaps  for  weeks  and 
then  die  of  peritonitis,  pleuritis  or  extensive  pus  formations 
(Fig.  3)  instead  of  perishing  within  twenty-four  hours  with 
septicaemia  as  they  would  if  they  had  not  been  protected  against 
this  organism.  In  chronic  cases  of  swine  plague,  as  found  in 
certain  outbreaks,  the  bacteria  are  often  attenuated  so  that 
when  inoculated  into  susceptible  rabbits  the  end  is  the  same  as 
when  the  rabbits  protected  by  partial  immunization  were  in- 
oculated with  virulent  cultures.  The  above  simple  formula 
which  was  worked  out  and  demonstrated  for  certain  swine  dis- 
eases seems  to  apply  to  infectious  diseases  generally. 

§  16.     Grouping   of  the   specific   infectious  diseases. 
It  will  be  found  in  the  study  of  the  morbid  anatomy  of  the 


A   MODIFIED   LESION 


23 


Fig.  3.  Large  abscess  in  partially  immunized  rabbit  caused  by  swine- 
plague  bacteria.  This  rabbit  lived  jji  days  after  its  inoculation  with  viru- 
lent swine  plague  bacteria.  At  death  its  weight  was  igSo  grams,  the  tumor 
itselj  weighing  goo  grams.  The  abscess  formed  dorsad  of  the  peritoneum. 
("a)  Caecum,  (b)  intestines,  {c)  abscess.  The  control  rabbit  of  same  weight 
and  age  died  of  septicaemia  in  16  hours. 


24  GROUPING    OF    INFECTIOUS    DISEASES 

various  specific  maladies  that  the  lesions  in  a  given  disease 
vary  in  different  species  and  in  individuals  of  the  same  species 
to  a  marked  degree.  This  fact  precludes  the  possibility  of 
classifying  or  arranging  them  after  their  morbid  anatomy,  if 
the  idea  of  a  specific  etiology  is  to  be  adhered  to.  If  the  infec- 
tious diseases  are  to  be  considered  as  parasitisms,  as  they  ap- 
pear to  be,  the  only  logical  method  of  classifying  them  accord- 
ing to  the  writer's  opinion,  is  the  one  suggested  by  their  eti- 
ology, namel}',  that  they  shall  be  placed  in  groups  according 
to  their  cause.  Thus  a  single  lesion  found  in  the  glands  of 
the  head,  in  the  lungs,  in  the  liver,  in  the  mesenteric  glands, 
in  the  skin,  in  the  joints,  or  in  the  generative  organs  would  be 
called  tubercular  if  the  bacteria  of  tuberculosis  could  be  demon- 
strated to  be  its  cause.  The  same  conclusion  would  be  main- 
tained regardless  of  the  character  of  the  lesion,  whether  cel- 
lular, purulent,  caseous  or  calcareous.  These  facts  are  enough 
to  suggest  that  the  most  direct  method  of  arranging  these  dis- 
eases for  purposes  of  .study  is  in  groups  composed  of  like  gen- 
eric etiological  factors. 

Most  of  the  known  specific  causes  of  the  infectious  dis- 
eases of  animals  are  bacteria.  It  is  necessary,  therefore,  to 
choose  from  among  the  numerous  classifications  one  to  be  fol- 
lowed in  grouping  the  diseases  according  to  the  genera  of  bac- 
teria producing  them.  Of  the  various  systems,  the  one  by 
Migula  seems  to  be  the  simplest  and  most  natural  and  conse- 
quently it  is  selected.  The  onl}^  radical  difference  between  it 
and  the  others,  so  far  as  pathology  is  concerned,  rests  in  the 
fact  that  the  old  genus  Baderhivi  is  revived,  but  with  a  new 
meaning.  All  rod-shaped,  non-motile  bacteria  are  placed  in 
this  genus.  This  causes  a  change  of  the  generic  name  from 
Bacillus  to  Bacterium  of  a  number  of  pathogenic  bacteria  such 
as  those  of  tuberculosis,  anthrax,  swine  plague  and  others  of  less 
importance. 

Following  the  bacterial  diseases  are  placed  those  caused 
by  higher  fungi.*     After  the  fungous  diseases  are  placed  those 


*The  number  of  diseases  included  in  this  work  that  are  caused  by 
fungi,  protozoa  and  higher  animal  parasites  are  so  few  that  they  have 
been  grouped  under  these  more  general  headings  rather  than  separated 
into  groups  of  the  same  generic  origin. 


CLASSIFICATION    OF    BACTERIA  25 

due  to  protozoa.  The  apparently  specific  diseases  for  which 
an  etiological  factor  has  not  been  demonstrated  are  grouped  to- 
gether after  those  of  recognized  cause.  Finally,  a  few  affections 
resulting  from  animal  parasites  are  appended  for  aid  in  differ- 
entiation from  infectious  diseases  that  they  somewhat  resemble 
in  their  lesions. 

§17.     Migula's  classification  of  bacteria.     The  genera 
are  included- of  the  first  three  families  only. 

FAMILIES. 

I.  Cells  globose  in  a  free  state, 
not  elongating  in  any  direc- 
tion before  division  into  1,2, 
or   3  planes i.   Coccacese. 

II.  Cells  cylindrical,  longer  or 
shorter,  and  onl}-  dividing  in 
I  plane,  and  elongating  to 
twice  the  normal  length  be- 
fore the  division. 

(i)  Cells  straight,  rod-shaped, 
without  sheath,  non-motile, 
or  motile  by  means  of  fla- 
gella 2.   Bacteriaceae. 

(2)  Cells  crooked,  without  sheath.  3.   Spirillacese. 

(3)  Cells  enclosed  in  a  sheath 4.  Chlamydobacteriacege. 

(4)  Cells    destitute   of    a    sheath, 

united  into  threads,  motile 
by  means  of  an  undulating 
membrane 5.    Beggiatoacese. 

GENERA. 

I .      Coccacecs. 

Cells  without  organs  of  motion. 

a.  Division  in  I  plane i.   Streptococcus. 

b.  Division  in  2  planes 2.    Micrococcus. 

c.  Division  in  3  planes 3.   Sarcina. 

Cells  with  organs  of  motion. 

a.  Division  in  2  planes 4.   Planococcus. 

b.  Division  in  3  planes 5.    Planosarcina. 


26 


CLASSIFICATION    OF    BACTERIA 


2 .  Baderiacece. 

Cells  without  organs  of  motion i.   Bacterium 

Cells  with   organs    of  motion  (fla- 
gellaj. 

a.  Flagella  distributed  over  the 

whole  body 2. 

b.  Flagella  polar 3. 

3.  Spirillacec? . 


Bacillus. 
Pseudomonas. 


Spirosoma. 


Cells  rigid,  not   snakelike  or    flex- 
uous. 

a.  Cells  without  organs  of  mo- 

tion     I 

b.  Cells  with  organs   of  motion 

(flagella). 

1.  Cells    with    one,    very 

rarely  2-3  polar   fla- 
gella    2.    Microspira 

2.  Cells  of  polar  flagella, 

in  tufts  of  from  5-20^   3. 
Cells  flexuous 4. 

REFERENCES. 


Spirillum. 
Spirochaeta. 


1.  Gay.  a  bacteriological  study  of  fistulous  withers,  botryomycosis 
and  infected  wounds  in  the  horse.  Atn.  Vet.  Review.  Vol.  XXIV. 
( 1901)  p.  877. 

2.  LucET.     Annals  de  V Institut  Pasteur.     Vol.  VI  ( 1893)  p.  324. 

3.  MiGULA.    System  der  Bacterien.     1897. 

4-  Moore.  Suppurative  cellulitis  in  the  limbs  of  cattle  due  to  strep- 
tococcus infection.     Am.  Vet.  Review.     June,  1898. 

5.  MooRE.  Observationsconcerning  the  significance  of  streptococci 
in  comparative  pathology.     Ant.  Vet.  Review.     Jan. -Mar.,  1900. 

6.  Moore.  Preliminary  observations  on  skin  disinfection  and  wound 
infection.     Am.  Vet.  Review.     Vol.  XXV.     ( 1901 )  p.  510. 

7.  NOCARD.  A  New  Pasteurellose  :  White  scours  and  lung  disease  of 
calves  in  Ireland.     Ayn.   Vet.  Review.     Vol.  XXV  (1901  )  p.  326. 

8.  Smith  and  Moore.  On  the  variability  of  infectious  diseases  as 
illustrated  by  hog  cholera  and  swine  plague.  Bulletin  No.  6.  U.  S.  Bureau 
0/ Animal  Industry.     1894.     p.  81. 

9.  Ward.  The  persistence  of  bacteria  in  the  milk  ducts  of  the  cows' 
udder.    Jour7ial  of  Applied  Microscopy.     Vol.  I.     (1898)  p.  205. 

10.  Ward.  The  invasion  of  the  udder  by  bacteria.  Bulletin  No. 
178  Cornell  Univ.  Agric  Exp  Station.     1900. 

ir.  WEiyCH.  General  bacteriology  of  surgical  infections.  Dennis' 
System  of  Surgery .     Vol.  I.     p.  249. 


CHAPTER   II. 


DISEASES  DUE    TO    STREPTOCOCCI. 


§  i8.  General  discussion  of  streptococci.  The  con- 
fusion which  exists  concerning  species  in  this  group  of  bacteria 
and  the  variety  of  antistreptococcic  serums  on  the  market,  ren- 
ders a  summary  of  the  present  knowledge  concerning  this  group 
of  bacteria  somewhat  desirable.  The  genus  Streptococcus  is  based, 
according  to  Migula,  on  its  method  of  reproduction  or  divi- 
sion. Streptococci  are  spherical  bacteria  which  divide  in  one 
plane.  The  segments  do  not  separate  but  are  held  together  in 
short  or  longer  chains,  although  the  divisions  seem  to  be  com- 
plete. Just  how  the  segments  are  held  together  is  not  fully  de- 
termined. According  to  older  and  more  commonly  encoun- 
tered classifications,  a  streptococcus  is  simply  a  number  of 
micrococci  (spherical  bacteria)  united  in  the  form  of  a  chain. 
In  some  of  the  supposedly  different  species  the  segments  are 
oblong  and  vary  in  size.  Frequently,  however,  the  segments 
vary  in  both  size  and  form  in  the  same  chain. 

The  more  usually  observed  cultural  characters  and  bio- 
chemic  properties  of  different  streptococci  are  quite  similar, 
although  it  is  difficult  to  obtain  two  cultures  that  will  exactly 
agree  in  all  of  their  manifestations  when  grown  on  a  large 
number  of  media.  Their  disease-producing  powers,  however, 
vary  within  wide  limits.  While  variations  in  the  physio- 
logical properties  and  pathogenesis  are  true  for  different  cul- 
tures (species?),  it  has  been  found  that  there  is  a  possibility  of 
much  variation  in  the  subcultures  of  the  same  species.  As 
with  certain  other  bacteria,  their  virulence  is  the  first  to  suffer 
change.  In  differentiating  species,  therefore,  the  fact  must 
not  be  overlooked,  that  the  existing  characters  and  properties 
possessed  by  the   streptococcus   in   hand,  may  have  been  more 


28  STREPTOCOCCI 

or  less  influenced  b}-  its  conditions  of  life.  When,  for  example, 
two  streptococci  appear  to  be  identical  under  the  majority  of 
tests,  a  slight  deviation  in  a  single  property  cannot  be  considered 
of  great  differential  value  especially  if  this  particular  manifesta- 
tion is  among  those  most  subject  to  change.  A  fundamental  diffi- 
culty in  differentiating  species  among  streptococci  seems  to  be  a 
lack  of  information  concerning  the  possible  variations  brought 
about  by  different  environments.  The  further  difficulty  of 
identifying  any  of  the  very  large  number  of  forms  which  have 
been  assigned  specific  names  is  due  to  the  brevity-  of  their  de- 
scription and  the  failure  of  the  author  to  mention  any  character 
or  property,  or   combination   of  the  same,  which  would  distin- 


•••  : 

•      1    <?^ 

/.    J      ) 

(•'•••/ 

1. 

2. 

5 

.''A^yy 

• 

••    V** 

•..•>:.r:.- 

.•••^* 

•     • 

••.                  . 

•••• 

• 

••••• 

G. 


Fig.  4.  Six'  forms  of  streptococci,  i .  Long  chains  consisting  of 
small  segments  arranged  with  equal  spaces  between  them.  2.  Long  and 
shorter  chains  in  which  the  segments  are  arranged  in  pairs.  The  size  of 
the  individual  segfnents  is  considerably  larger  than  those  in  the  long 
chains,  j.  Short  and  longer  chains  where  the  segments  are  oi'al  zvith  the 
lotig  diameter  perpendicular  to  the  long  axis  of  the  chain.  4.  Long 
interlacing  chains.  5.  Short  and  longer  chains  with  one  or  tnore  seg- 
ments very  much  larger  than  the  others.  6.  Chains  shozving  divisions 
in  two  planes.  This  form  of  division  has  been  observed  i7i  a  few  cases. 
The  dividing  in  two  planes  is  an  exception  which  is  not  satisfactorily 
explained    .  X  about  1000. 


CLASSIFICATION  29 

guisli  it  from  others.  However,  such  deficiencies  cannot  well 
be  avoided  in  the  time  of  rapid  accumulation  of  observations 
and  the  evolution  of  methods. 

§  19.  Classification  of  streptococci,  A  few  investi- 
gators have  tried  to  eliminate  the  confusion  concerning  species 
by  classifying  streptococci  according  to  distinct  morphologic 
characters  and  pathogenic  properties.  Of  these  classifications 
the  following  may  be  mentioned  : 

I.  The  classification  of  von  Lingelshei^n.  This  author  di- 
vides all  streptococci  into  two  groups,  or  species,  namely  : — 

(a)  Streptococcus  brevis — which  is  non-pathogenic. 
((^)   Streptococcus  longus — which  is  pathogenic. 

This  is  a  combination  of  pathogenesis  and  morphology 
which  the  author  thought  applicable  to  the  entire  genus.  He 
worked  very  largely,  however,  with  the  streptococci  from  the 
human  mouth  and  throat. 

II.  The  classification  of  Kiwth.  Kurth  worked  largely 
with  the  streptococci  from  cases  of  scarlatina.  His  system  is 
practically  the  same  as  that  of  von  Lingelsheim,  with  the  ex- 
ception that  he  does  not  include  pathogenesis  as  necessarily 
belonging  to  either  group.     The  divisions  are  as  follows  : 

ia)  Streptococcus  rigidi — Streptococci  growing  in  short 
chains,  and  which  impart  a  uniform  turbidity  to  bouillon. 

(b)  Streptococcus  flexuosi — Streptococci  which  grow  in  long 
interlacing  chains  which  form  flocculi  in  bouillon  leaving  the 
liquid  clear. 

III.  The  classification  of  Pasquale .  Pasquale  worked  with 
thirty-three  streptococci,  including  nearly  all  of  the  then  known 
species.  His  work  was  quite  exhaustive,  but  he  had  to  deal 
wnth  cultures  of  various  generations.  He  divides  them  into 
four  groups,  as  follows  : 

{a)  Short  saphrophytic  streptococci. 

i^b)  Long  non- virulent  streptococci. 

(£■)   I^fOng  pathogenic  streptococci. 

(flf)  Short  highly  infectious  streptococci. 

Group  (yd)  pertains  largely  to  bacteria  which  are  no  longer 
recognized  as  streptococci,  for  example,  the  diplococcus  (yl//<:r£'- 
coccus  lanceolatus)  of  pneumonia.      It  is  now  known  that  strep- 


30  STREPTOCOCCI    IN    NATURE 

tococci  which  grow  in  short  chains  are  often  virulent.     This  is 
especially  true  of  the  pyogenic  forms. 

The  study  of  streptococci  from  various  sources,  more  espe- 
cially from  tissues  of  diseased  animals,  suggests  the  desirability 
of  delaying  a  further  classification  until  more  definite  data  are 
obtained  concerning  the  natural  history,  not  only  of  these,  but 
also  of  the  species  normally  present  on  the  mucous  membranes 
of  animals,  and  in  nature  generalh'.  The  specific  name  is, 
pathologically  or  even  biologically  speaking,  of  little  moment 
unless  we  can  attach  a  certain  definite  meaning  to  it  concern- 
ing the  morphologic  characters,  cultural  manifestations  and  the 
degree  of  disease-producing  power  possessed  by  the  organism 
designated.  In  a  group  of  twenty-eight  streptococci  previ- 
ously studied,  the  writer  found  the  pathogenic  forms,  /.  e. ,  those 
able  to  produce  disease  in  rabbits,  guinea  pigs,  or  mice,  about 
equally  divided  between  the  long  and  the  short  chains.  Of 
the  twenty-eight,  nine  possessed  a  certain  amount  of  virulence 
for  one  or  more  of  these  animals. 

§  20.  Distribution  of  streptococci  in  nature.  The 
fact  has  been  pointed  out  in  many  publications  that  strepto- 
cocci are  quite  widely  distributed  in  nature.  The  results  of 
the  bacteriologic  examinations  of  normal  mucous  membranes 
show  that  they  are  frequently  included  in  the  bacterial  flora  of 
the  mouth,  throat,  nares,  intestines,  vagina,  and  in  a  few  cases 
they  have  been  found  in  the  bronchioles  of  the  horse  and  rab- 
bit. They  are  also  present  in  greater  or  less  numbers  on  the 
skin,  especially  in  the  deeper  layers,  presumably  in  the  ducts 
of  the  sweat  and  sebaceous  glands  and  along  the  hair  shafts 
and  follicles.  The}'  exist  in  soil  and  in  water,  and  occasionally 
these  forms  are  quite  as  delicate  in  their  morphology  and 
equally  as  sensitive  to  the  influence  of  environment  as  those 
isolated  from  diseased  animal  tissues.  In  view  of  this  wide 
distribution,  the  presence  of  a  streptococcus  in  any  abnormal 
condition  cannot  be  considered  necessarily  a  specific  infection 
from  a  previous  case  of  the  same  kind.  In  many  affections 
where  the  specific  organism  has  been  demonstrated,  such  for 
example  as  diphtheria,  tuberculosis,  and  hog  cholera,  strepto- 
cocci frequently  appear  in  the  lesions.    In  these  cases,  they  are 


STREPTOCOCCI    IN    NATURE  3I 

considered  as  accidental  or  secondary  invaders,  although  in 
some  of  these  maladies,  such  as  tuberculosis,  they  are  believed 
to  be  of  more  or  less  secondary  importance.  When,  however, 
the  specific  cause  of  the  disease  is  not  positively  known,  and 
streptococci  which  possess  certain  pathogenic  powers  for  ex- 
perimental animals  are  constantly  present  and  seem  to  stand  in 
a  causal  relation  to  the  disease,  the  pathologist  is  confronted 
with  a  puzzling  problem  in  trying  to  determine  the  source  and 
the  etiological  importance  of  the  organism  in  hand.  In  cases  of 
infection  leading  at  once  to  septicaemia,  peritonitis  or  suppura- 
tion, the  explanation  is  more  simple  than  in  the  epizootic  dis- 
eases, such  as  Brustseuche ,  where  the  constant  presence  of  strep- 
tococci in  the  lesions  can  be  quite  as  easily  explained  on  the 
ground  of  their  invasion  of  the  parts  affected  from  a  normal 
habitat  as  on  the  hypothesis  of  a  specific  infection.  It  is  in 
these  instances  that  we  are  seeking  for  the  crucial  test. 

We  have  found  in  a  few  test  experiments  that  when  certain 
of  the  delicate  streptococci  which  exist  (are  found)  in  external 
nature  (soil  or  water)  are  introduced  within  the  tissues  of  cer- 
tain animals  they  become,  by  reason  of  their  activities,  a  source 
of  irritation  which  causes  local  tissue  disturbances.  In  a  few 
cases  they  have  produced  septicaemia  with  fatal  results. 

In  cases  of  infection  resulting  in  septicaemia,  or  in  those 
where  the  disease  is  more  localized,  as  in  strangles  or  mastitis, 
and  possibly  in  others  where  the  affection  spreads  more  or  less 
rapidly,  we  cannot  well  escape  from  the  feeling  that  the  strep- 
tococci, present  in  such  large  numbers,  must  either  stand  in  a 
causal  relation  to  the  disease  or  be  accounted  for  bj^  their  rapid 
proliferation  in  native  soil  made  favorable  for  their  excessive 
increase  by  the  conditions  produced  by  the  true  etiological  fac- 
tors. Their  natural  distribution  is  so  wide,  and  their  virulence 
so  capricious  that  a  secondary  invasion,  which  seems  always  to 
be  possible,  renders  the  fixing  of  etiological  responsibility  upon 
a  streptococcus  isolated  from  any  diseased  tissue  a  somewhat 
difficult  task.  The  problems  in  this  connection  which  concern 
us  most  and  which  need  more  extended  investigation  pertain 
(i)  to  the  determination  of  the  parasitic  possibilities  of  strepto- 
cocci existing  in  nature  /.  e.,  those  ordinarily  considered  as  sap- 


32  STREPTOCOCCI    IN    NATURE 

rophytes  and  (2)  to  the  distinction,  if  it  exists,  between  strep- 
tococci which  are  able  to  produce  local  inflammatory  processes 
leading  to  suppuration  and  those  which  produce  highly  infective 
and  rapidly  spreading  diseases,  such  as  erysipelas  and  strangles. 

In  view  of  the  confusion  respecting  species  in  this  genus, 
the  identity  of  streptococci  isolated  from  the  lesions  in  the 
various  diseases  which  have  been  attributed  to  streptococci  is, 
at  the  present  time,  a  matter  of  some  uncertainty.  There  is 
also  considerable  skepticism  concerning  the  primary  etiological 
significance  of  the  streptococci  in  a  number  of  diseases  in  which 
they  have,  heretofore,  been  assigned  as  the  cause.  Recent  in- 
vestigations, especially  those  of  Lignieres,  tend  to  the  conclu- 
sion that  they  are  often  secondary  invaders  in  certain  of  these 
diseases.  Petruschky  has  pointed  out  analogous  cases  in 
human  infections  in  showing  that  streptococci  play  an  impor- 
tant role  as  secondary  invaders  in  human  diphtheria,  scarlatina 
and  tuberculosis. 

In  the  absence  of  verified  results  to  prove  the  non-specific 
relation  of  streptococci  to  the  diseases  which  have  with  reason- 
able certaintj'  been  attributed  to  the  activities  of  this  genus  of 
bacteria,  these  affections  are  tentatively  included  among  the 
specific  streptococci  maladies.  It  is  very  important,  especially 
when  the  use  of  antistreptococcic  serums  are  in  question,  to 
take  into  account  the  apparently  large  number  of  forms,  or 
species,  commonly  included  in  the  general  statement  of  a  strep- 
tococcus disease  or  infection.  In  1897,  Van  de  Velde,  in  a  very 
exhaustive  series  of  experiments,  showed  that  one  strepto- 
coccus antitoxin  will  not  immunize  against  another  save  to  a 
very  slight  degree. 

REFERENCES. 

1.  Klein.  Seventeenth  Annual  Report  of  the  Local  Government 
board.  Supplement  contai?ii?ig  report  of  Aledicat  Officers.  London. 
1887.     P256. 

2.  KuRTH.    Arbeiten   a.  d.  Kaiserlichen  Gesimdheitsainte,  Bd.  VII, 

(i89i),S.  389. 

3.  Moore.  Bulletin  JVo.j.'  U.  S.  Bureau  of  Animal  Industry. 
Washington,  D.  C.      1893.     p.  9. 

4.  Pasqu.^le.  Beitrdge  zur  path.  Anal.  11.  zur  allgenieinen  Path- 
ologie,  Bd.  XII  (1893).  S.  433. 

5.  Petruschky.    Zeitschrift  f.  Hygiene.     Bd.  XVII.     S.  59. 

6.  VON  LiNGELSHEiM.     Zeitschrift  f.  Hygiene,  Bd.  X.   1891,  S.  331. 

7.  Welch.  The  Am.  four,  of  the  Med.  Sciences.  Vol.  CII.  (1891). 
P-  439- 


INFECTIOUS    DISEASES  33 

STRANGLES 

§  21.  Characterization. ^Strangles  is  an  infectious  dis- 
ease of  horses,  asses  and  their  hybrids  occurring  sporadically 
and  in  epizootics.  It  is  characterized  principally  by  a  fever, 
followed  by  an  acute  catarrh  of  the  mucosa  of  the  upper  air 
passages  especially  of  the  nares,  and  a  suppurative  inflamma- 
tion of  the  lymph  glands  of  the  submaxillary  and  pharyngeal 
regions.  The  lesions,  however,  are  not  restricted  to  these 
parts.      It  is  a  disease  of  3'oung  animals. 

§22.  History.  Strangles  was  among  the  first  equine  dis- 
eases to  be  recognized.  In  1664,  vSolleysel  gives  an  account  of 
it  and  points  to  the  fact  that  it  had  been  known  for  a  long 
time.  Its  infectious  (contagious)  nature  was  determined  ex- 
perimentally in  1790  by  Lafosse  and  since  that  time  by  a  num- 
ber of  other  investigators.  In  1873,  Rivolta  found  in  the  pus 
of  the  abscesses  a  micrococcus  which  appeared  in  chains  of 
from  three  to  five  segments.  Baruchello,  in  1887,  described 
as  its  cause  an  organism,  which  he  designated  as  Bacillus 
adenitis  equi.  Strangles  has  been  thought  by  some,  to  be 
identical  with  scrofula  and  measles.  Sacco  and  Na.sbot  consid- 
ered it  as  horse  pox.  Viborg  and  Toggia  and  more  recently 
Nasbot  advocated  the  inoculation  of  horses  with  the  lymph  of 
horse  pox  as  a  prophylactic  measure  against  strangles.  Dela- 
motte  demonstrated  that  this  procedure  was  of  little  or  no  pre- 
ventive value.  The  supposed  specific  cause  {Streptococcus 
equi)  of  strangles  was  described  first  by  Schiitz  and  later  by 
Sand  and  Jensen  in  the  same  year  (1888).  The  discovery  has 
been  confirmed  by  Poels,  L,upka,  and  others.  More  recently 
Lignieries  has  discovered  a  "coccobacillus"  which  he  believes 
to  be  the  primary  cause.  He  considers  the  streptococcus  of 
Schiitz  as  a  secondary  invader  of  no  specific  value. 

§23.  Geographical  distribution.  Strangles  is  a  wide 
spread  disease  among  horses.  It  appears  to  stand  in  equine 
pathology  very  much  as  measles  do  in  human  medicine^a 
disease  of  early  life  and  consequently  more  prevalent  where 
there  are  more  young.  It  seems  to  exist  in  all  countries 
where  the  horse  kind  are  raised  and  to  be  more  prevalent  in 
breeding  districts  than   elsewhere. 


34  STRANGLES 

§  24.  Etiology.  Strangles  is  supposed  to  be  caused  by 
Streptococcus  equi,  first  described  by  Schiitz  in  1888.  With 
pure  cultures  of  this  organism  Schiitz  was  able  to  produce  the 
disease  in  healthy  horses.  It  is  fatal  to  mice,  a  maximum  viru- 
lent virus  destroying  life  in  three  days. 

Lignieres,  who  had  exceptionally  good  opportunities  in 
1895-96  for  studying  the  disease,  found  and  identified  the 
streptococcus  of  Schiitz.  However,  he  concluded  from  his  in- 
vestigations that  the  cause  of  the  disease  was  a  coccobacillus 
which  he  isolated  with  some  difficulty.  He  found  that  this 
organism  soon  escaped  from  the  tissues  but  that  it  "places 
the  animal  organism  in  an  extraordinary  state  of  susceptility 
with  regard  to  extraneous  bacteria,  notably  streptococci."  On 
this  ground,  he  explains  the  almost  constant  presence  of  strep- 
tococci in  the  lesions  of  this  disease.  The  results  need  to  be 
confirmed. 

§  25.  Symptoms.  The  first  indication  of  this  disease 
is  a  rise  of  temperature.  There  is  loss  of  appetite,  depres- 
sion, and  often  great  weakness.  The  general  symptoms  may 
continue  for  a  few  days  before  the  localization  of  the  lesions 
is  apparent.  The  first  local  manifestation  consists  usually  in  a 
catarrh  of  the  nasal  mucosa  or  swelling  of  the  sub-maxillary 
and  pharyngeal  lymphatic  glands.  The  nasal  discharge  is  at 
first  serous  and  somewhat  viscid,  but  in  from  3  to  5  days  it  be- 
comes purulent  and  of  a  yellowish  green  color.  The  catarrhal 
condition  may  exist  in  one  or  both  nostrils.  It  maj^  extend 
into  the  pharynx,  larynx,  trachea  and  even  to  the  bronchi. 
In  most  cases,  swelling  of  the  sub-maxillary  glands  appears 
concurrently  with  the  purulent  nasal  catarrh.  The  swelling 
is  hot  and  painful  when  pressed.  The  spreading  of  the  in- 
flammation to  the  connective  tissue  which  surrounds  the  glands, 
and  the  stasis  of  the  lymph  in  the  efferent  lymph  vessels,  often 
cause  the  development,  from  the  sub-maxillary  lymph  glands, 
of  very  extensive  swellings  that  may  occupy  the  entire  inter- 
maxillary space,  and  may  spread  even  to  the  outer  side  of  the 
maxilla.     In  most  cases  abscesses  form. 

In  exceptional  cases,  strangles  may  present  catarrhal 
symptoms  without  suppuration    of  the  lymph  glands.     Jensen 


MORBID    ANATOMY  35 

states  that  it  may  first  assume  the  form  of  pharyngitis,  purulent 
pneumonia,  and  pleuritis  without  any  well-marked  morbid 
affection  of  the  lymph  glands.  The  urine  generally  remains 
alkaline;  it  frequently  contains  a  considerable  quantity  of  al- 
bumen. 

At  times,  strangles  is  accompanied  by  a  cutaneous  exan- 
thema which  takes  the  form  of  an  eruption  of  wheals,  nodules, 
vesicles,  and  even  pustules  may  appear,  chiefly  on  the  sides  of 
the  neck,  shoulders,  and  sides  of  the  chest.  These  exanthe- 
mata are  characterized  by  their  sudden  appearance,  and  often 
by  their  equally  rapid  disappearance.  An  eruption  of  vesicles 
may  break  out  on  the  nasal  raucous  membrane.  The  contents 
of  the  vesicles  is  at  first  limpid,  but  later  it  becomes  purulent. 
Rabe  states  that  the  streptococcus  of  strangles  can  produce 
ulcers  on  the  nasal  mucous  membrane. 

§  26.  Morbid  anatomy.  The  lesions  in  strangles  are 
interesting  from  the  fact  that  in  the  beginning  the  disease  is 
general  but  later  in  its  course  it  becomes  a  series,  exceedingly 
variable  in  different  individuals,  of  localized  morbid  foci. 
The  lymphatic  glands  seem  to  suffer  most,  although  any  organ 
may  be  involved.  As  indicated  by  the  symptoms,  the  lesions 
in  most  cases  are  characterized  by  an  acute  inflammatory  pro- 
cess followed   by  suppuration. 

The  glandular  swellings  about  the  head  usually  terminate 
in  suppuration,  the  pus  discharging  either  externally  or  into 
the  oral  cavity.  In  other  cases,  the  pus  undergoes  caseation. 
Frequently  the  inflamed  glands  become  confluent,  resulting  in 
a  single  large  abscess.  Small  abscesses  may  occur  under  the 
pharyngeal  mucosa. 

The  inflammation  may  extend  to  the  superficial  lymph 
vessels  of  the  skin,  especially  of  the  head,  resulting  ui  the  for- 
mation of  a  large  number  of  small  abscesses.  This  may  be 
followed  by  a  diffuse  phlegmonous  swelling  of  the  parts. 
Metastatic  abscesses  are  liable  to  occur  in  a  great  variety  of 
organs.  The  metastasis  seems  to  take  place  through  both 
lymph  and  blood  vessels  although  the  lymphatic  glands  are 
most  often  affected.  Suppurating  foci  have  been  described  in 
nearly  every    lymphatic  gland  in  the  body.     The  discharge  of 


36  STRANGLES 

pus  from  the  bronchial,  mesentric  or  other  glands,  within  or 
adjacent  to  the  pleura  or  peritoneal  cavities,  may  give  rise  to 
a  fatal  pleuritis  or  peritonitis.  There  seems  to  be  no  part  of 
the  bod}'  free  from  possible  suppurative  lesions  as  a  result  of 
metastasis. 

Strangles  may  become  chronic,  especially  when  the  nasal 
catarrh  extends  into  the  sinuses  of  the  head,  in  the  guttural 
pouches,  or  pharyngeal  cavity.  In  these  cases  the  animal 
becomes  emaciated.  The  lesions  in  these  cases  resemble  some- 
what those  of  chronic  glanders. 

Death  from  strangles  is  caused  usually  by  either  septi- 
caemia, pyaemia,  pleuritis,  peritonitis  or  suppurating  (metas- 
tatic) pneumonia. 

Many  complications  are  liable  to  arise.  Mixed  infections 
or  secondary  diseased  conditions  often  occur.  The  prognosis, 
however,  is  favorable.  The  statistics  collected  from  the  Euro- 
ropean  armies  show  a  mortality  not  exceeding  three  per  cent. 

§  27.  Differential  diagnosis.  Strangles  is  to  be  differ- 
entiated from: 

(i)  Purulent  nasal  catarrh.  In  this  affection,  there  is 
rarely  suppurating  submaxillary  glands  although  occasionally 
these  glands  may  be  swollen. 

(2)  From  glanders.  In  glanders,  the  tissue  changes  are 
more  persistent  and  the  skin  lesions,  if  they  exist,  do  not  heal 
as  rapidly  as  in  strangles.  In  chronic  cases,  the  diagnosis  is 
quite  difficult.  Here  animal  inoculations  must  be  resorted  to. 
Mice  inoculated  subcutaneously  with  the  nasal  discharge  suc- 
cumb to  the  streptococcus  of  strangles  but  they  are  resistant 
to  the  bacterium  of  glanders.  Guinea  pigs  inoculated  in  a 
like  manner  will,  in  case  of  glanders,  develop  that  disease  (§ 
105)  from  the  lesions  of  which  pure  cultures  of  Bacteruim 
mallei  ma}-  be  obtained. 

(3)  From  parotitis.  In  this  affection  the  swelling  is 
localized  and  suppuration  does  not  often  occur. 

(4)  Abscesses  due  to  pyogenic  bacteria.  The  cases  are 
rare  where  there  would  be  any  question  as  to  diagnosis.  The 
bacteriological  examination  including  the  inoculation  of  animals 
would   give   positive   aid   unless   the   pyogenic  organism  hap- 


EQUINE    PLEURO-PNEUMONIA  37 

pened  to  be  a  virulent  streptococcus  in  which   case  a   differen- 
tiation might  be  impossible. 

REFERENCES. 

T.  LiGNiERES.  The  etiology  of  equine  influenza  or  infectious 
pneumonia.  The  Jour,  of  Conip.  path,  and  Therapeutics  Vol.  XI  (i8g8) 
p.  J12.     Translated  from  Recueil  de  Med.  Vet.  Vol.  IV.  (1897). 

2.  Poles  Die  Mikrokokken  der  Druse  des  Pferdes.  fort.  der. 
Med.  Bd  VI  (1888)  S.  4. 

3.  Reeks.    Intracranial  strangles,  abscess  in  a  mare.      77?^  Jour,  of 
Comp.  path,  and  Therap.  Vol  XII  (1899)   p  178. 

4.  Sand  and  Jensen.  Die  Aetiologie  der  Druse.  Deutsche  Zeit. 
fur.   Thier  Med.  Bd.  XIII  (  1888)  S.  437. 

5.  SCHUTZ.  Der  Streptococcus  der  Druse  der  Pferdes.  Arch.  fur. 
ThierheilkundeBA.^lV  (1888)  S.   172. 


EQUINE   CONTAGIOUS   PLEURO-PNEUMONIA. 

§  28.  Characterization.  The  disease  known  as  conta- 
gious pneumonia  or  contagious  pleuropneumonia  in  the  horse 
is  characterized  by  a  high  temperature,  rapid  pulse,  but  occa- 
sionally without  definite  lung  disturbances.  lyike  strangles, 
both  the  symptoms  and  the  lesions  vary  to  such  a  degree  that 
it  is  difficult  to  single  out  diagnostic  features.  This  disease  is 
known  in  France  diS  pneumoenteritis  and  in  Germany  as  Brust- 
seuche. 

§29.  History.  In  earlier  times,  influenza  and  contagious 
pleuro-pneumonia  of  the  horse  were  not  distinguished  as  sepa- 
rate diseases.  Falke  differentiated  the  disease  formerly  known 
as  influenza  into  contagious  pleuro-pneumonia  and  influenza. 
Since  his  time  they  have  been  recognized  as  distinct  diseases. 

§  30.  Geographical  distribution.  Contagious  pneu- 
monia, like  strangles,  is  widely  distributed.  It  appears  in  epi- 
zootic form  although  in  certain  places  it  is  reported  to  be  almost 
constantly  present.  It  prevails  most  extensively  where  large 
numbers  of  horses  are  congregated.  It  has  frequently  been 
reported  as  the  cause  of  much  trouble  among  the  horses  in  the 
European  armies.  In  the  eastern  part  of  the  United  States,  it 
appears  from  time  to  time  in  more  or  less  serious  epizootics. 


38  EQUINE    PLEURO-PNEUMONIA 

It  is  quite  common  among  horses  shipped  from  the  West.      In 
these  cases,  it  is  designated  as  "western"  or  "stable"  fever. 

§  31.  Etiology.  There  is  some  question  concerning  the 
specific  cause  of  this  disease.  A  large  number  of  suspected 
microorganisms  have  been  isolated  and  described,  but  the 
Streptococcus  of  Schiitz  seems  to  be  the  only  one  with  which 
the  disease  has  been  produced  experimentally. 

In  1887,  Schiitz  published  the  results  of  his  investigations 
into  the  cause  of  Brustseuche.  He  described  an  organism 
which  appeared  as  a  diplococcus  in  tissues,  but  in  bouillion  cul- 
tures it  grew  in  flocculi.  From  the  description,  it  appears 
that  this  organism  was  a  streptococcus  notwithstanding  the 
fact  that  in  the  tissues  it  appeared  more  often  as  a  diplococcus. 
In  cultures,  he  speaks  of  it  as  chains  growing  in  masses.  He 
mentions  a  capsule,  but  in  the  cases  described  it  does  not  seem 
to  be  invariably  present  and  it  is  not  mentioned  in  prepara- 
tions made  from  cultures.  Chantemesse  and  Delamotte,  Gal- 
tier  and  Violet,  and  Cadeac  found  streptococci  in  the  lesions 
of  animals  suffering  from  this  disease.  Although  differences 
seem  to  exist  in  the  streptococci  isolated  and  studied  by  these 
investigators,  there  is  a  striking  similarity  between  them.  It 
is  not  at  all  unlikely  that  difference  in  methods  may  explain 
the  variations  mentioned. 

According  to  Schiitz,  cultures  inoculated  into  horses  pro- 
duce the  disease  when  injected  directly  into  the  lungs  by 
means  of  a  hypodermic  syringe.  The  resulting  contagious 
pleuro-pneumonia  exhibts  the  same  symptoms  and  runs  a  like 
course  to  those  observed  in  cases  of  the  disease  contracted  in 
the  natural  or  common  manner.  The  essential  changes  shown 
on  post-mortem  examination  were  multiple  gangrenous  patches 
in  the  lungs  with  parenchymatous  degeneration  of  the  most 
important  organs.  The  inoculated  streptococci  were  found 
in  the  tissues  of  the  artificially  produced  disease.  i\ccording 
to  Schiitz,  the  bacteria  of  contagious  pleuro-pneumonia  are 
found  most  numerously  in  the  lungs  or  the  exudate  on  the 
pleurae.  They  are  also  met  with  in  the  nasal  discharge  and 
in  expired  air  (Rust).  Nothing  positive  is  known  concerning 
the  life  history   of  the   streptococci   outside  the    animal    body. 


ETIOLOGY  39 

They  are  supposed  not  to  be  able  to  live  longer  than  six  weeks 
within  the  animal  body  ;  but  in  certain  cases,  especially  in  en- 
cysted deposits  in  the  lungs,  the  virus  may  remain  active  for  a 
much  longer  time. 

Baumgarten  and  Hell  oppose  the  view  that  Schiitz's  strep- 
tococcus is  specific,  while  Rust  aud  Fiedler  support  it.  Hell 
maintains  that  with  our  present  means  of  investigation,  the 
bacteria  of  contagious  pleuro-pneumonia  cannot  be  differen- 
tiated from  the  pyogenic  streptococci  or  from  the  strepto- 
coccus of  erysipelas.  In  fact,  Hell  believes  that  the  strepto- 
coccus of  Schiitz  has  a  pathogenic  effect  in  horses  affected 
with  pleuro-pneumonia;  but  as  there  is  no  positive  proof  of 
its  being  specific,  he  maintains  that  we  are  justified  in  sup- 
posing that  this  ubiquitous  micro-organism  has  only  an  injuri- 
ous influence  on  the  course  of  the  disease,  contributing  to  the 
production  of  the  secondary  lesions.  Hell  further  states  that 
protective  inoculation  with  Schiitz's  bacteria,  which  at  first 
promised  good  results,  has  not  proven  to  be  satisfactory. 
Fiedler,  on  the  other  hand,  has  obtained  the  same  bacteriolo- 
gical results  and  has  arrived  at  the  same  conclusions  as  Schiitz. 
He  also  states  that  he  has  experimentally  produced  pleuro- 
pneumonia in  a  horse  by  inoculation  of  cultivations  of  these 
bacteria. 

Lignieres  (See  §  24)  believes  that  his  cocco-bacillus 
stands  in  an  etiological  relation  to  this  disease  and  that  here 
as  in  strangles  the  streptococcus  is  a  secondar}'  invader. 

The  writer  made  a  bacteriological  examination  of  the 
organs  from  five  cases  of  fatal  contagious  pneumonia  of  the 
horse.  In  each  case,  the  lungs  were  more  or  less  hepatized, 
but  the  other  organs  were  nearly  normal  in  appearance. 
Without  exception,  a  streptococcus  appeared,  usually  in  pure 
culture,  from  the  lungs.  The  inoculated  media  from  the  other 
organs,  liver,  spleen,  and  kidney  remained  clear.  The  strep- 
tococci isolated  from  the  different  cases  were  identical  in  their 
morphology  and  cultural  manifestations  and  pathogenesis. 
A  microscopic  study  of  the  lungs  from  the  different  horses 
showed  micrococci  singly,  in  pairs  and  occasionally  in  short 
chains.     Distinct    capsules  were    not  observed.     In    bouillon 


40  EQUINE    PLEURO-PNEUMONIA 

cultures,  however,  the}'  appeared  in  long  chains,  leaving  the 
liquid  clear,  as  described  by  Schiitz. 

This  streptococcus  did  not  grow  in  gelatin,  or  on  serum,  or 
on  potato.  It  would  not  develop  in  acid  media.  On  agar,  the 
colonies  were  small  and  characteristic  of  streptococci,  i.  e., 
with  a  thickened,  convex,  grayish  center  surrounded  by  a 
thin,  spreading  bluish  border,  nearly  equal  in  width  to  the 
diameter  of  the  central  portion.  It  fermented  dextrose,  lac- 
tose and  saccharose,  with  the  formation  of  acids  but  no  gas. 
Milk  remained  unchanged  in  appearance. 

In  mice  and  rabbits,  it  produced  a  rapidly  fatal  .septicaemia, 
but  guinea-pigs  were  unaffected.  A  horse  inoculated  in  the 
pleural  cavity  with  a  small  quantity  of  the  culture  was  killed 
lo  days  later.  At  the  point  of  inoculation  and  extending 
over  an  area  equal  to  one-half  of  the  lung,  there  were  strong 
adhesions  between  the  lung  and  parietes.  The  subjacent  lung 
tissue  was  hepatized.  Pure  cultures  of  the  streptococcus  were 
obtained  from  the  exudate  and  from  the  hepatized  lung. 

Although  a  few  discrepancies  exist  between  the  descrip- 
tion of  Schiitz's  organism  and  this  streptococcus,  in  the  more 
essential  features  they  seem  to  be  identical.  The  cases  were 
examined  before  the  publication  of  Lignieres'  results,  and  the 
methods  emploj'ed  did  not  meet  the  requirements  of  those 
used  in  isolating  his  cocco-bacillus.  Although  a  very  careful 
histological  study  of  the  pneumonic  tissue  was  made,  Lig- 
niere's  organism  was  not  detected. 

§  32.  Symptoms.  The  period  of  incubation  is  given 
as  varying  from  one  to  fourteen  days,  but  usually  from  four 
to  ten  days  elapse  from  the  time  of  exposure  to  the  de- 
velopment of  the  first  .symptoms.  The  symptoms  vary  to  a 
marked  degree.  When  pneumonia  develops  early  in  its 
course,  the  disease  may  appear  suddenly  ;  and,  in  addition  to 
the  elevation  of  temperature,  there  is  cough  and  difficult 
breathing.  Often  the  .symptoms  differ  from  those  of  fibrinous 
pneumonia  by  the  absence  of  distinct  evidences  of  local  lesions 
which  are  found  in  that  disease.  The  first  regular  symptom 
is  a  rapidly  increasing  temperature  frequenth'  accompanied 
by  a  chill.     The   pulse   rate   is  increased.     There   is   general 


MORBID    ANATOMY  4 I 

depression,  usually  loss  of  appetite  and  muscular  weakness: 
the  conjunctivae  and  other  visible  mucous  membranes  become 
congested.  There  ma}^  be  from  the  beginning  marked  indica- 
tions of  localized  lesions  in  the  lungs,  or  the  general  symptoms 
maj'  continue  without  evidence  of  pronounced  lung  disturb- 
ance. The  duration  of  the  disease  depends  almost  entirely 
upon  its  cour.se.  In  the  more  typical  cases,  the  fever  lasts 
from  5  to  8  days.  The  period  of  convalesence  is  much  longer 
lasting  from  two  to  three  weeks.  Many  symptoms  may  be 
exhibited  corresponding  to  the  variations  in  the  morbid  pro- 
cesses. If  the  heart,  digestive  tract,  liver,  kidneys  or  brain 
become  the  localized  seat  of  the  disease,  symptoms  referable 
to  impaired  functions  of  these  organs  are  in  evidence.  The 
,  septicaemic  form  has  been  described  as  being  followed  by 
localized  suppurative  lesions. 

§  33.  Morbid  anatomy.  The  morbid  changes  in  the  tis- 
sues and  organs  vary  according  to  the  course  of  the  disease, 
which  is  exceedingly  irregular.  It  may  exhibit  a  regular  form 
of  lobar  inflammation  of  the  lungs  or  the  disease  may  run  an 
atypical,  complicated,  acute,  chronic,  and  not  infrequentl}-  an 
abortive  course.  Further,  authorities  agree  that  many  com- 
plications may  arise  modifying  or  changing  completely'  the 
morbid  anatomy  of  the  disease  from  the  conditions  found  in 
the  more  typical  cases.  In  the  few  cases  examined  post  mor- 
tem by  the  writer,  the  gross  lesions  were  restricted  to  the  lungs. 
They  were  either  in  a  state  of  congestion,  or  exhibited 
changes  of  fibrinous  pneumonia  in  the  cephalic  (anterior) 
portions  of  one  or  both  organs.  Pneumonia  is  the  most  com- 
mon localized  lesion.  Several  quite  distinct  forms  of  lung 
disturbances  are  described. 

In  the  lobular  form  of  pleuro-pneumonia  which  is  stated 
furnishes  the  largest  number  of  subjects  for  a  post  mortem  ex- 
amination, there  is  a  multiple  haemorrhagic,  gangrenous 
pneumonia  with  secondary  pleuritis  and  possibly  parenchy- 
matous degeneration  of  the  vital  organs  of  the  body.  Areas 
of  the  lung  tissue  of  greater  or  less  size  are  thickened  and 
hepatized.  These  are  located  more  especially  near  the  base  of 
the    lungs  and  in   the  lower  (ventral)  portions.      Bright    foci 


4.2  EQUINE    PLEURO-PNEUMONIA 

which  are  distinctly  defined  from  the  neighboring  tissues  are 
scattered  through  the  hepatized  areas  and  appear  on  the  sur- 
face of  sections  of  the  hepatized  parts.  Usually,  several  of  these 
foci  are  present.  They  vary  in  size  from  a  millimeter  to  20  or 
more  centimeters  in  diameter.  In  recent  lesions,  these  areas 
are  very  small,  of  a  greyish- red  color  and  surrounded  by  a 
grayish  zone  consisting  of  leucocytes  (limited  reactionary  in- 
flammation). In  more  advanced  lesions,  they  become  yellow- 
ish, necrotic  and  finally  cavities  varying  from  the  size  of  a  pea 
to  that  of  a  hen's  egg.  These  cavities  are  surrounded  by  a 
smooth  capsule.  There  are  other  foci  which  contain  greasy, 
foetid,  watery  pus  (gangrene  of  the  lungs),  by  reason  of  the 
necrotic  parts  of  the  lung  undergoing  liquefaction  in  conse- 
quence, it  is  stated,  of  the  admittance  of  air.  The  lungs  often 
contain  suppurating  foci  composed  of  a  whitish  pus  mixed 
with  necrotic  lung  tissue.  It  sometimes  happens  that  the  foci 
just  described  are  absent  in  the  lungs,  although  during  life 
distinct  symptoms  of  such  a  localized  affection  may  have  been 
present.  In  these  cases,  it  is  assumed  that  absorption  of  the 
necrotic  tissue  has  taken  place.  The  remaining  tissue  of  the 
lungs  is,  more  or  less,  hyperaemic  and  oedematous. 

The  pleurae  show  signs  of  a  diffuse,  exudative  pleuritis, 
the  starting  point  of  which  in  the  large  majority  of  cases,  is 
from  necrotic  deposits  which  are  situated  in  the  periphery  of 
the  lungs.  Pleuritis  may  occur,  however,  apparently  as  a 
primary  lesion  without  the  necrotic  foci  being  present.  The 
contents  of  a  necrotic  deposit  in  the  lungs  rarely  breaks 
through  into  the  pleural  cavity.  In  some  cases,  the  visceral 
and  costal  layers  of  the  pleura  are  congested,  diffusely  or  in 
spots,  and  are  sprinkled  with  haemorrhages.  Frequentl}'  the 
pleurae  are  covered  with  soft  red  granulations  covered  with 
soft,  yellowish  layers  of  exudate  which  are  partly  membranous 
and  partly  coagulated  in  a  reticular  manner,  and  which  can  usu- 
ally be  easily  removed.  The  pleural  cavities  generally  contain 
a  considerable  quantity  of  fluid.  Dieckerholf  states  that  from 
30-40  liters  of  a  serous  fluid  are  occasionally  present.  The 
exudate  is  usually  turbid  and  of  an  orange,  greyish-red,  brown- 
ish-red, or  dirty-greyish  color.     It  is  generally  mixed  with  nu- 


MORBID    ANATOMY  43 

merous  yellowish  colored  flakes  which  form  a  sediment  when 
the  liquid  is  allowed  to  stand  in  a  glass.  The  pleuritic  exudate 
sometimes  consists  of  pure  pus  and  less  frequently  of  blood. 
The  pleuritic  exudate  when  present  in  large  amount  com- 
presses the  lungs  and  pushes  them  away  from  the  thoracic 
walls.  In  cases  of  recovery,  the  pleuritic  exudate  may  be- 
come organized,  binding  the  lungs  to  the  costal  walls  and  dia- 
phragm. Various  forms  of  fibrous,  villous  growths  develop 
on  the  pleurae. 

The  records  show  that  the  other  organs  of  the  body  are 
usually  in  a  state  of  parenchymatous  inflammation  and  fatty 
degeneration.  The  muscular  tissue  of  the  heart  is,  as  a  rule, 
brownish-grey  in  color,  .soft  and  suffers  from  cloudy  swelling. 
In  severe  cases,  it  shows  well-marked  fatty  degeneration,  is  of 
a  clay  color,  and  is  occasionally  infiltrated  with  a  large  number 
of  small,  yellowish-white  foci.  The  liver  is  enlarged,  of  a 
cla}'  color  or  sometimes  icteric,  and  presents  signs  of  fatty  de- 
generation. The  spleen  is  flaccid,  its  pulp  increased  and  often 
sprinkled  with  haemorrhages.  The  kidneys  ma}'  be  swollen, 
friable  and  sometimes  show  numerous  haemorrhagic  foci. 
The  lymph  glands,  especially  the  bronchial  and  mediastinal 
glands,  are  enlarged,  softened,  and  exhibit  on  section  a  greyish- 
red  color.  The  muscles  of  the  body  are  soft,  and  of  a  yellow- 
ish-brown color.  Small  haemorrhages  under  the  serous  mem- 
branes are  frequently  reported.  Slight  endocarditis  ma}' 
occur.  The  blood  is  said  to  suffer  less  change  than  any  of 
the  solid  organs. 

The  mucous  membrane  of  the  stomach  and  intestines  is 
frequently  hyperaemic,  swollen,  sprinkled  with  haemorrhages, 
and  sometimes  even  ulcerated.  The  bronchial  mucous  mem- 
brane is  also  swollen  and  inflamed. 

In  other  cases,  the  lesions  are  those  of  lobar  pneumonia,  in 
which  the  stages  of  hyperaemic,  red  hepatization,  grey  hepa- 
tization and  resolution  (in  favorable  cases)  follow  each  other 
in  regular  order.  In  a  fatal  case  postmortemed  by  the  writer 
the  right  lung  was  entirely  involved,  the  left  one  being  but 
slightly  hyperaemia.  In  non-fatal  cases,  the  crisis  is  reached 
on  the  5  or  6  day,  after  which  resolution  begins. 


44  SEPTICAEMIA    IN    CHICKENS 

As  already  stated  the  lesions  in  this  disease  are  so  exceed- 
ingh'  variable  that,  in  addition  to  the  more  typical  pneumonia, 
almost  any  modification  can  be  found.  The  detailed  descrip- 
tion of  many  of  these  variations  as  described  by  Dieckerhofif 
are  worthy  of  careful  study. 

§34.  Differential  diagnosis.  This  disease  is  to  be  dif- 
ferentiated from  (  I )  influenza,  with  which  it  is  often  confused, 
(2)  simple  pneumonia  following  colds,  and  (3)  the  result  of 
foreign  substances  introduced  into  the  V:)ronchi. 

REFERENCES. 

1.  Cadeac.    Contribution  a  I'etiologie  de  la  pneumonia  contagieuse 
du  cheval.     Conip.  Rend,  de  la  Soc.  de  Biol.     1889.     p.  316. 

2.  Fleming.    Infectious  pneumonia  of  the  horse.      The  Velerinary 
Jour.      Vol.  XXXIII  p.  I. 

3.  SchIttz.     Die  Ursache  der   Brustseuche  der  Pferde.      Virchow's 
Archives.     Bd.  CVII.     S.  356. 

4.  SCHUTZ.      Die  genuine  Lungenentziindung  der  Pferde.     Archiv 
fur  Wissen.  u.  prak.   Thierheilkunde.     Bd.  VIII. 

5.  SiEDAMGROTZKY.     Ueber  infectiose  Pneumonien    bei    Pferden. 
Deutsche  Med.   Wochenschrifl.     18S2.     S.  668. 

6.  Williams.     Contagious  pleuro-pneumonia  of   the  horse.     Am. 
Vel.   Reviexv.     Vol.  XVI  ( 1892)  p.  301. 


APOPLECTIFORM  SEPTICAEMIA  IN   CHICKENS. 

§  35.  Characterization.  A  rapidly  fatal  septicaemia 
in  chickens  caused  by  a  streptococcus. 

§  36.  History.  This  disease  was  recently  discovered 
and  described  by  Norgaard  and  Mohler.  xA-lthough  the  symp- 
toms and  lesions  given  correspond  somewhat  closel}'  to  those 
mentioned  by  Mazza  and  Rabieux,  there  is  a  marked  differ- 
ence in  the  etiological  factor.  This  newly  discovered  disease 
is  based  upon  the  findings  and  investigations  following  a 
single  epizootic  among  fowls.  Thus  far  it  has  not  been  identi- 
fied in  any  other  locality. 

§  37.  Geographical  distribution.  The  only  locality 
from  which  it  has  been  described  is  lyOudoun  Co.,  Va. 

^  38.  Etiology.  This  disea.se  is  stated  to  be  due  to  a 
streptococcus  which  grows  in  short  or  longer  chains  with  seg- 
ments varying  from  0.6  to  cSyw  in  diameter.      In  some  cases 


MORBID    ANATOMY  45 

elongated  forms  are  observed.  It  is  an  aerobe,  and  a  faculta- 
tive anaerobe.  When  cultivated  on  artificial  media  it  does  not 
liquefy  gelatin,  it  does  not  change  the  appearance  of  milk,  but 
causes  slight  acidity  and  thickening  of  the  lower  stratum  with- 
out coagulation  of  the  casein.  The  reaction  of  alkaline  bouil- 
lon is  changed  to  an  acid  one  and  it  does  not  give  a  visible 
growth  on  potato.  It  stains  by  Gram's  and  Gram-Weigert's 
method.  In  bouillon  it  grows  in  somewhat  flaky  masses  while 
the  medium  remains  clear.  It  was  fatal  to  fowls,  mice,  rabbits 
and  swine  ;  guinea  pigs,  dogs  and  sheep  were  not  destroyed  by 
inoculation.  This  organism  has  not  been  given  a  specific 
name. 

§  39-  Symptoms.  It  is  not  at  all  uncommon  to  find  the 
fowls  dead  and  lying  under  the  roosts.  Occasionally  capons 
were  observed  to  be  sick  for  from  12  to  24  hours  prior  to 
death.  In  these  cases  the  feathers  become  rufiied  and  the  fowl 
showed  evidence  of  extreme  depression.  The  onset  of  the  dis- 
ease is  very  sudden  and  its  course  a  very  rapid  one,  usually 
terminating  in  death. 

§  40.  Morbid  anatomy.  The  authors  describe  the  mor- 
bid anatomy  as  follows  :  "The  spleen  is  more  or  less  enlarged, 
showing  hyperplasia  of  the  Malphigian  corpuscles.  The  pulp 
contains  numerous  areas  of  extravasated  blood.  When  a  stained 
section  is  examined  by  means  of  a  hand  lens  a  number  of  cir- 
cular semi-transparent  foci,  the  size  of  a  pin  hole,  may  be  noted. 
These  are  found  on  microscopic  examination  to  be  centers  of 
necrobiosis,  consisting  of  parenchyma  which  has  undergone 
coagulation  necrosis,  and  surrounded  by  a  more  or  less  well 
defined  capsule  of  embryonic  and  further  developed  connective 
tissue  cells  and  filaments. 

On  microscopic  examination,  the  kidneys  show  slightly 
swollen  epithelial  cells  of  a  beginning  parenchymatous  degen- 
eration to  the  well  pronounced  disintegration  of  the  renal 
epithelium  of  acute  nephritis.  The  degree  of  degeneration 
depends,  as  a  rule,  upon  the  course  of  the  disease.  If  a  bird 
succumbs  suddenly  or  in  the  course  of  a  few  hours  the  morbid 
changes  are  either  not  apparent  at  all  or  but  slightly  pro- 
nounced, while,  on  the   other  hand,  the   duration   of  three  or 


48  SWINE   PLAGUE 

animal.  On  account  of  its  frequent  association  with  hog 
cholera,  it  has  been  thought  by  some  investigators,  more 
especially  Billings,  Welch  and  Clements,  to  be  a  secondary 
affection  only.  In  1895,  the  writer  investigated  several  out- 
breaks of  this  disease  in  Southern  Minnesota  where  it  occurred 
uncomplicated  with  hog  cholera.  More  recently  two  epi- 
zootics of  swine  plague  have  been  studied  in  New  York  State, 
where  no  evidence  was  found  of  its  being  a  secondary  infection 
but    where    in   every  particular    its    independent    nature    was 

indicated. 

§  45.  Geographical  distribution.  Swine  plague  is  a 
wide  spread  disease  in  this  country.  It  seems  to  occur  more 
or  less  frequently  in  every  state  in  the  Union.  It  is  quite 
widely  distributed  in  Germany,  but  to  what  extent  it  exists  in 
other  countries  there  is  little  or  no  available  evidence. 

^  46.  Etiology.  Swine  plague  is  caused  by  a  non-motile 
elongated,  oval  bacterium   described   by  Smith  in  1886.     It  is 

identical  with  the  bacillus  of  Schweineseuche 
described  by  Loeffler  in  1885.  Hueppe  pro- 
posed the  name  Baderhim  {Bacillus)  septi- 
caemiae  licmo?-rliagicae  for  this  organism. 

The  bacterium  of  swine  plague  and  its 
varieties  have  not  been  systematically  stud- 
ied and  classified.     It  is  of  interest  to  note, 
Fig.  5.    Baderi-  however,  that   the   bacteria  of  rabbit  septi- 
nm  of  swine  plague,  ^^^j^^j^^    ^^^^    cholera   and   wildseuche    are 

thought  to  be  identical  with  it. 

The  pathogenic  organism  associated  with  the  lesions  in 
certain  forms  of  broncho-pneumonia  in  cattle  differs  very 
slightly  from  this.  In  human  pathology,  we  find  a  striking  re- 
semblance in  Micrococcus  lanceolatus  to  the  swine-plague  bac- 
terium, especially  in  its  manifold  and  varied  pathogenic  possi- 
bilities and  its  existence  in  human  saliva. 

In  grouping  these  bacteria,  the  fact  should  be  recognized 
that  experimentally  they  are  not  interchangeable  in  their 
pathogenesis  except  for  the  rabbit.  Thus  an  epizootic  form 
of  fowl  cholera  has  not  been  produced  with  the  swine  plague 
or  rabbit  septicaemia   organism.      Further,  it   has  been  shown 


ETIOLOGY  49 

that  in  the  upper  air  passages  of  healthy  swine,  cattle,  horses, 
cats  and  dogs*  there  are  bacteria  not  distinguishable  in  their 
cultural  characters  and  their  effect  upon  rabbits  from  the  swine- 
plague  bacterium.  The  presence  of  this  organism  in  the  trachea 
of  healthy  pigs  has  been  suggested  as  the  source  of  the  cause 
of  sporadic  cases  of  swine  plague  and  it  may  explain  the  fre- 
quent association  of  this  form  of  pneumonia  with  hog  cholera. 
What  the  conditions  are  by  which  these  bacteria  are  enabled 
to  produce  disease  in  their  host  have  not  been  clearly  pointed 
out. 

If  the  rabbit  is  taken  as  the  animal  on  which  to  test  the 
pathogenesis  of  the  bacteria  belonging  to  the  swine-plague 
group,  we  find  that  those  from  different  sources  are  very  simi- 
lar. In  nature,  the  bacteria  of  swine  plague,  rabbit  septicaemia, 
fowl  cholera,  and  those  located  in  the  normal  upper  air  pas- 
sages of  the  various  species  of  animals  mentioned  possessed 
of  marked  variation  in  virulence  exist,  that  is,  those  which 
will  kill  a  rabbit  when  inoculated  subcutaneously  with  a  pure 
culture  in  from  i6  to  24  hours  to  those  which  require  from  3 
to  10  days,  or  even  weeks,  to  destroy  life.  With  the  variations 
in  the  time  period,  we  have  corresponding  differences  in  the 
lesions.  The  virulent  forms  produce  septicsemia  while  the 
attenuated  varieties  excite  a  severe  purulent  infiltration  about 
the  place  of  inoculation  and  exudates  on  one  or  more  of  the 
serous  membranes.  Conversely,  it  has  been  shown  that  rab- 
bits possessed  of  a  certain  amount  of  natural  or  artificially 
produced  resistance  will,  when  inoculated  with  a  virulent  cul- 
ture, die  after  the  same  period  of  time  and  with  lesions  similar 
to  those  produced  by  the  attenuated  virus  in  the  susceptible 
rabbit. 

The  fact  that  this  organism  is  not  frequently  described  in 
our  works  on  bacteriology  and  because  of  some  coniusion 
existing  concerning  it  and  the  bacillus  of  hog  cholera,  it  is 
deemed  best  to  insert  a  short  description  of  it  here. 


*The  investigations  thus  far  made  show  these  bacteria  to  be  present 
in  48  per  cent,  of  healthy  swine,  80  per  cent,  of  cattle,  50  per  cent,  of 
sheep,  16  per  cent,  of  horses,  90  per  cent,  of  cats,  and  30  per  cent,  of  dogs. 


50  SWINE    PLAGUE 

§  47.     Brief   description  of   the  bacterium  of  swine 
plague. 

Morphology. — A  non-motile,  rod-shaped  organism  varying  from  0.8 
to  2.0  microns  in  length  and  from  0.4  to  1.2  microns  in  breadth.  The 
ends  are  oval,  and  the  shorter  forms  resemble  micrococci.  The  size 
depends  upon  the  medium  and  the  stage  of  development  of  the  individ- 
ual bacteria.  A  capsule  has  not  been  demonstrated,  although  often 
there  appears  to  be  one  in  preparations  made  directly  from  tissues.  It  is 
not  observed  in  cultures.  Spores  have  not  been  seen.  Involution  forms 
are  not  uncommon  in  old  cultures.  They  are  especially  numerous  in 
the  organs  of  a  rabbit  when  it  is  allowed  to  lie  for  some  hours  after 
death,  before  it  is  examined.  It  exhibits,  when  stained  in  cover-glass 
preparations  made  directly  from  animal  tissues,  a  light  center  with 
deeply  stained  extremities  (polar  stain).  In  preparations  made  directly 
from  cultures  this  character  is  much  less  marked.  It  stains  readily  with 
the  basic  aniline  dyes.  It  does  not  retain  the  coloring  matter  when 
stained  after  Gram's  method. 

Cultural  and  biocheinic  properties. — This  organism  is  less  hardy 
than  the  bacillus  of  hog  cholera,  and  on  certain  of  the  media  used  it 
grows  very  feebly  or  not  at  all.  It  requires  a  temperature  of  about  37^* 
C.  although  it  develops  very  slowly  at  the  room  temperature. 

Agar. — The  growth  on  this  medium  is  not  vigorous.  It  is  of  a  neu- 
tral grayish  color,  with  a  glistening,  moist  appearing  surface.  It  is 
slightly  viscid  and  adheres  to  the  agar  surface.  Isolated  colonies  vary 
from  I  to  2  mm.  in  diameter,  nearly  round,  convex,  with  smooth  and 
sharply-defined  margins.  The  condensation  water  becomes  faintly 
clouded  with  a  grayish  sediment  which  becomes  viscid.  Within  the 
agar  the  colonies  appear  as  minute  grayish  dots.  In  agar,  especially  in 
plates  (Petri  dishes),  it  emits  a  peculiar,  disagreeable,  pungent  odor. 

Gelatin. — Ordinarily  it  does  not  grow  in  gelatin.  (Dr.  Theobald 
Smith  found  that  certain  cultures  grew  in  this  medium. ) 

Potato. — It  does  not  grow  on  potato. 

Bouillon. — Alkaline  peptonized  bouillon  becomes  uniformly  clouded 
in  24  hours  when  kept  at  a  temperature  of  36°  C.  Occasionally  cultures 
are  obtained  in  which  the  growth  appears  in  the  form  of  flocculent 
masses,  but  usually  after  a  few  generations  these  disappear  and  the 
liquid  becomes  uniformly  cloudy.  If  the  bouillon  contains  any  dextrose 
or  muscle  sugar,  its  reaction  becomes  acid  in  24  to  48  hours,  owing  to 
the  fermentation  of  the  carbohydrate.  With  the  virulent  cultures  the 
liquid  clears  within  a  few  daj's.  The  small  amount  of  grayish  sediment 
becomes  viscid  after  some  days,  and  upon  agitation  it  is  forced  up, 
appearing  as  a  somewhat  twisted  tenacious  cone,  with  its  apex  at  or  near 
the  surface  of  the  liquid.  Frequently  a  thin,  grayish,  somewhat  viscid 
band  composed  of  bacteria  is  found  on  the  sides  of  the  tube  at  the  sur- 
face of  the  liquid.     It  will  not  grow  in  acid  bouillon.     If  the  bouillon 


BACTERIUM  OF  SWINE  PLAGUE  5 1 

contains  from  i  to  2  per  cent,  glucose,  the  growth  is  slightly  more 
vigorous. 

Effect  on  sugars. — In  the  fermentation  tube,  alkaline  bouillon  con- 
taining sugars  become  uniformly  clouded  in  both  branches.  Gas  is  not 
produced.  In  bouillon  containing  dextrose  and  saccharose  the  reaction 
becomes  strongly  acid  in  24  hours,  but  the  reaction  of  alkaline  bouillon 
containing  lactose  is  not  changed. 

Milk. — Milk  inoculated  with  this  organism  remains  unchanged  in 
appearance  for  several  weeks.  When  boiled,  after  this  period,  the 
casein  is  not  coagulated. 

Indol. — This  organism  grows  feebly  in  Dunham's  solution  ;  some 
cultures  have  given  a  decided  indol  reaction,  but  others  have  not.  The 
production  of  indol  is  reported  to  be  one  of  the  properties  of  the  German 
swine  plague.  Smith*  obtained  only  a  trace  of  indol  in  one  out  of  four 
cultures  of  swine-plague  bacteria. 

Phenol. — This  was  found  by  Lewandowski's  t  method  in  all  of  the 
cultures  tested  by  Smith.  I  have  failed  to  obtain  the  reaction  in  a  few 
cultures,  but  usually  it  appears. 

Thermal  death  point. — This  organism  is  destroyed  in  bouillon  at 
58°  C.  in  ten  minutes.  A  temperature  of  56°  C.  for  this  time  did  not 
destroy  its  vitality. 

Effect  of  drying.  — These  Vjacteria  can  not  stand  drying.  The  bacteriam 
in  a  drop  of  bouillon  dried  on  a  cover-glass  and  kept  at  the  room  tem- 
perature are  destroyed  in  24  to  36  hours.  In  similar  preparations  made 
from  agar  cultures  they  resist  drying  from  five  to  eight  days.  The  dif- 
ference in  the  time  between  the  two  cultures  is  probably  due  to  the 
thicker  layer  in  case  of  the  agar  preparations. 

Persistence  of  vitality  iti  ivater  and  soil. — Experiments  to  determine 
the  length  of  time  this  organism  will  live  in  water  and  in  the  soil  show 
that  it  is  destroyed  in  water  in  test  tubes  in  from  nine  to  eleven  days. 
In  the  soil  it  was  not  found  after  eight  days.  Dr.  Smith  states  that  it  is 
destroyed  in  the  soil  after  four  days. 

Power  to  resist  disinfectants. — The  bacterium  of  swine  plague  is  very 
sensitive  to  the  action  of  disinfectants.  A  large  number  of  these  agents 
have  been  tested.     The  following  are  among  the  more  important : 

Commercial  sulphuric  acid,  ^s  per  cent,  kills  in  30  minutes. 

Commercial  sulphuric  acid,  '4'  per  cent,  kills  in  10  minutes. 

Lime,  lime  water  kills  in  i  minute. 

Lime,  0.015  pc  cent,  kills  in  30  minutes. 

Carbolic  acid,  }i  per  cent,  kills  in  60  minutes. 

Carbolic  acid,  i  per  cent,  kills  in  5  minutes. 

Carbolic  acid,  2  per  cent,  kills  in  i  minute. 


*Special  report  on  swine  plague,  1891,  p.  89. 
tDeutsche  nied.  Wochenschrift,  1890,  s.  11 86. 


52  SWINE    PLAGUE 

Formalin,  solution  1-2000  kills  in  5  minutes. 

Trikresol,  ji  per  cent,  kills  in  5  minutes. 

Pathogenesis. — This  organism  is  pathogenic  for  rabbits,  guinea  pig» 
and  mice  among  the  smaller  experimental  animals  and  for  swine.  With 
the  virulent  form  rabbits  inoculated  either  subcutaneously  or  in  the  vein 
with  very  small,  o.ooi  c.  c.  doses,  die  of  septicaeemia  in  from  16  to  24 
hours.  Guinea  pigs  are  slightly  less  susceptible.  When  inoculated  sub- 
cutaneously with  0.1  to  0.2  c.  c.  of  a  bouillon  culture,  they  die  in  from 
30  to  72  hours.  Mice  succumb  in  about  24  hours  when  inoculated  with 
a  drop  of  the  culture.  Pigs  inoculated  intravenously  usually  die  from 
acute  septicaemia  in  from  18  to  36  hours.  If  they  live  longer  there  may 
be  decided  lung  lesions.     (See  report  on  swine  plague.  Smith.) 

§  48.  Symptoms.  It  is  frequently  difficult  to  recognize 
symptoms  distinctive  of  swine  plague.  The  peculiarities  of 
swine  render  it  exceedingly  difficult  to  obtain  evidence  on 
physical  examination  of  lung  disease.  Sometimes  this  affec- 
tion runs  a  very  rapid  course,  the  animal  dying  of  septicaemia. 
Usually  it  is  more  protracted,  lasting  from  a  few  days  to  a 
week  or  longer.  Animals  affected  with  the  more  chronic  form 
where  there  are  lung  lesions,  eat  very  little,  or  refuse  food 
altogether.  They  cough  considerably,  especially  when  forced 
to  run.  The  back  is  usually  arched  and  the  groins  sunken. 
The  whites  of  the  eyes  are  reddened.  The  skin  over  the  ventral 
surface  of  the  body,  nose  and  ears  is  frequently  flushed.  The 
cough,  however,  is  the  most  reliable  indication  we  have  of 
swine  plague  ;  but  in  some  cases  of  hog  cholera  the  coexistence 
of  broncho-pneumonia  also  causes  the  animal  to  cough  when 
forced  to  move  rapidly. 

i^  49.  Morbid  anatomy.  There  are  many  known  varia- 
tions in  the  appearance  of  the  internal  organs  of  hogs  which 
have  died  of  swine  plague.  The  characteristic  lesions  are,  as 
previously  stated,  to  be  found  in  the  lungs.  Frequently  the 
abdominal  viscera  appear  to  be  normal  although  a  careful 
examination  will  usually  reveal  slight  changes.  In  the  lungs, 
however,  the  disease  is  usually  obvious. 

The  variety  of  lesions  produced  by  the  inoculation  of  swine- 
plague  bacteria  is  not  so  great  as  that  observed  in  the  naturally 
contracted  disease.  While  there  are  outbreaks  in  which  con- 
siderable uniformity  is  observed,  there  are  others  in  which 
each  animal  is  a  surprise  to  the  pathologist.     In  general  it  may 


MORBID    ANATOMY 


53 


be  stated  that  the  hmgs  and  the  digestive  tract  are  the  chief 
seats  of  the  disease,  though  other  organs,  notably  the  lymphatic 
glands,  are  secondarily  involved.  The  disease  is  localized  in 
the  lungs  and  in  the  digestive  tract  most  likely  because  the 
bacteria  gain  entrance  through  the  respiratory  and  digestive 
passages. 

The  lungs  have  been  found  dis- 
eased in  nearly  every  outbreak  which 
has  been  investigated.  In  some  out- 
breaks the  lung  lesions  predominated 
and  pneumonia  was  the  direct  cause  of 
death.  In  individual  cases,  pneumonia 
is  absent  but  pleuritis  and  interlobular 
oedema  are  genearlly  present.  In  a 
few  instances  interlobular  emphysema 
of  the  lungs  has  been  observed. 
With  pneumonia  the  ventral  lobes  are 
first  attacked,  then  the  cephalic  and 
azygos,  and  lastly  the  principal  lobes. 
This  movement  of  the  disease  seems  to 
depend  on  gravity,  inasmuch  as  the 
diseased  parts  are  marked  off  from  the 
healthy  portion  by  a  nearly  horizontal 
line.  In  other  words,  the  most  depend- 
ent portions  of  the  lungs  are  the  ones 

„  _    _  ,  IT  portion  of  lung  showing  in- 

affected  first,  and  as  the  disease  pro- ^^^,,^^ .^,^  ^.^^^ ^;^^  .„^^,,^^^,^. 

gresses  upwards  only  a  small  portion  /<„-  spaces  with  serum  and 
of  the  principal  lobe  directly  under  the  lymph. 
back  of  the  animal,  remains  pervious,  provided  the  life  of  the 
animal  is  maintained  up  to  this  point.  In  nearly  all  cases  of 
pneumonia  in  swine  the  disease  involves  the  regions  described 
which  are  indicated  in  the  cut  by  shading.  In  exceptional 
cases,  where  the  disease  is  caused  by  lung  w^orms  or  due  to  em- 
bolism, the  pneumonia  involves  portions  of  the  principal  lobes 
not  contiguous  to  the  ventral  lobes. 

Two  kinds  of  pneumonia  are  encountered,  lobar  and 
catarrhal  or  broncho-pneumonia.  In  the  former  the  vesicular 
portion  of  the  lung  substance  is  chiefly  affected  ;  in  the  latter 


Fig.  6.     Section   of    a 


54 


SWINE    PLAGUE 


the  smaller  bronchioles  are  said  to  be  primarily  affected  and 
the  vesicular  portion  or  alveoli  secondarily.  In  croupous 
pneumonia,  there  is,  following  the  stage  of  congestion,  an 
emigration  of  red  blood  corpuscles,  some  leucocytes  and  an 
exudate  of  fibrin  into  the  air  spaces.  These  elements  are 
firmh'  matted  together  by  the  coagulating  fibrin,  making  the 
diseased  lung  firm  to  the  touch.  In  broncho-pneumonia  the 
catarrhal  condition  of  the  smaller  air  tubes  makes  them  imper- 
vious to  air.  The  lung  tissue  which  they  supply  is  gradually 
emptied  of  air  and  assumes  the  appearance  of  red  flesh,  owing 
to  the  collapse  of  the  walls  of  the  alveoli  and  the  distended 
condition  of  the  capillary  network.  vSubsequently  the  inflam- 
mation extends  into  the  alveoli,  which  then  become  distended 
with  cellular  masses. 


Fig.  7.     Portion  of  hmg  showing  emphysema. 

The  nature  of  the  lung  disease  will  depend  more  or  less 
upon  the  mode  of  entrance  of  the  virus.  If  it  entered  only 
by  w^ay  of  the  air  tubes  it  will  appear  perhaps  as  a  broncho- 
pneumonia. If  it  enters  the  lung  tissue  through  the  circu- 
lation we  may  have  more  or  less  scattered  centers  of  hepatiza- 
tion'fembolic  pneumonia.)     If  it  enters  by  way  of  the  pleura. 


MORBID    ANATOMY 


55 


the  virus  will  creep  along  the  interlobular  and  peribronchial 
tissue  before  it  invades  the  parenchyma  proper. 


P'iG.  8.  Right  lung  of  pig.  The  stippled  portion  is  usually  involved 
i7i  cases  of  infectious  pneumonia  or  S7vine  plague,  {b)  cephalic  lobe,  [c)  ven- 
tral lobe,  [a]  principal  lobe.  The  ventral  lobe  is  usually  the  seat  of  the 
more  advanced  disease  and  consequently  the  first  to  becoDie  hepatized.  The 
cephalic  portion  of  the  principal  lobe  (.r)  is  usually  hepatized  and  the 
remaining  portion  deeply  reddened. 

In  natural  infection  the  swine-plague  bacteria  seem  to 
enter  the  lung  tissue  chiefly  by  way  of  the  air  tubes.  At  the 
same  time  it  is  not  improbable  that  occasionally  the}'  may 
enter  the  serous  cavities  first,  z.  e.,  invade  the  pleural  cavities 
and  thence  the  lungs.  This  probability  is  shown  by  inocula- 
tions in  which  intravenous  injections  produced  exudative  pleu- 
ritis,  and  pneumonia  of  the  most  dependent  portions  of  the 
lungs  covered  by  the  pleural  exudate.  It  is  not  improbable 
that  even  in  the  natural  disease  the  bacteria  which  have 
gained  access  to  a  portion  of  the  lung  tissue  by  way  of  the  air 
tubes  reach  the  pleura  covering  this  portion,  and  may  then  b}- 
this  route  invade  other  portions  of  the  lungs.  It  may  be  that 
in  this  way  a  pneumonia  originally  single  may  become  double. 
It  has  been  observed  that  the  first  pneumonic  infiltration  of 
the  principal  lobe  was  at  the  points  of  contact  with  the  dis- 


56  SWINE   PLAGUE 

eased  ventral  lobe,  and  that  the  resting  of  a  lobe  against  an  in- 
flamed serous  surface,  such  as  the  pericardium,  caused  a  pneu- 
monic infiltration  at  the  point  of  contact. 

The  character  and  seat  of  the  lung  lesions  are  somewhat 
variable.  It  is  difficult  to  find  two  lungs  exactly  alike  so  far 
as  gross  appearances  go.  This  to  be  sure  may  be  due  largely 
to  the  fact  that  animals  die  in  different  stages  of  the  disease. 
Yet  there  are  differences  evidently  not  dependent  on  this  fact 
which  must  be  left  for  special  pathological  investigation. 

In  general  the  cephalic  (anterior)  half  of  a  swine-plague 
lung  is  hepatized,  of  a  dark-red  or  grayish-red  color  and  firm 
to  the  touch.  The  pleura  is  more  or  less  thickened  and 
opaque,  and  possibly  covered  with  easily  removable,  friable, 
false  membranes.  In  the  more  recently  affected  regions  a 
faint  but  quite  regular  delicate  mottling  with  yellow  is 
observed  to  shine  through  the  pleura  when  not  thickened. 
These  minute  hazy,  yellowish  dots  usually  occur  in  groups  of 
four.  Occasionally  whitish  or  yellowish  patches  varying 
much  in  size  are  seen  perhaps  more  frequently  in  the  ventral 
lobes.  These  correspond  to  homogeneous  dead  masses  of  lung 
tissue. 

When  such  lungs  are  cut  open,  the  section  presents  much 
the  same  appearance,  both  as  regards  color,  and  mottling,  as 
when  viewed  from  the  surface,  excepting  that  the  details  are 
less  distinct.  In  some  cases  in  the  most  recently  invaded  ter- 
ritories in  the  principal  lobe  and  nearer  the  dorsum  in  the 
other  lobes,  the  dark  or  grayish-red  cut  surface  shows  grayish 
lines  usually  arranged  in  curves  and  circles.  These,  so  far  as 
determined,  represent  the  cut  outlines  of  the  interlobular  and 
peribronchial  tissue  infiltrated  with  cells.  It  has  already  been 
stated  that  these  lines  ma}^  represent  the  paths  along  which 
the  swine-plague  bacteria  invade  the  lungs  from  the  pleural 
surface. 

The  cut  ends  of  the  bronchi  of  the  ventral  lobes  are  fre- 
quently occluded  with  thick,  whitish  pus  ;  in  the  other  lobes 
a  reddish  froth  is  usually  present.  Rarely  they  also  contain 
thick  glairy  mucus  in  which  particles  of  dry  pus  and  lung 
worms  are  imbedded.     The  contents  of  the  air  tubes  in  the 


MORBID    ANATOMY  57 

ventral  lobes  may  have  been  derived  from  the  overdistended 
alveoli,  or  else  a  broncho-pneumonia,  may  have  preceded  the 
swine-plague  pneumonia. 

In  microscopic  sections  of  diseased  lung  tissue  the  alveoli 
and  smallest  air  tubes  are  found  distended  with  cell  masses 
consisting  chiefly  of  leucocytes.  Usually  there  is  very  little 
fibrin  and  ver}'  few  red  corpuscles  in  the  alveoli,  even  in  cases 
in  which  the  disease  was  quite  recent.  It  may  be  that  the 
stage  represented  in  ordinary  croupous  pneumonia  by  the  pres- 
ence of  fibrin  in  connection  with  the  cellular  elements  is  very 
brief,  and  that  it  is  speedily  replaced  by  large  numbers  of  leu- 
cocytes. The  large  predominence  of  these  elements  in  some 
portions  of  the  lungs,  as  well  as  beginning  fatty  degeneration, 
is  probably  the  cause  of  the  regular  mottling  of  the  lungs,  as 
seen  from  the  surface.  The  little  yellowish  hazy  dots  represent 
alveoli  surrounded  by  the  hyperaemic  walls. 

The  necrotic  and  caseous  changes  so  frequent  in  swine 
plague  are  most  interesting.  The  latter  are  usually  quite  small 
and  disseminated  in  large  numbers  over  the  diseased  lobes. 
The  former  represent  larger  masses  from  a  marble  to  a  horse- 
chestnut  in  size.  They  represent  tissue  which  has  been  des- 
troyed by  the  rapid  multiplication  of  swine-plague  bacteria  in 
particular  localities.  Hence  the}-  are  found  in  all  stages  of  the 
pneumonia.  The  large  caseous  masses  may  be  considered  as 
the  result  of  a  slow  death  of  larger  areas  of  lung  tissue,  due 
primaril}'  to  the  gradual  overdistention  of  the  tissue  by  leuco- 
cytes, and  hence  the  gradual  cutting  off  of  the  blood  supply. 
One  is  a  rapid  death  due  -directh-  to  highly  virulent  bacteria, 
the  other  a  slow  death,  or  a  kind  of  dry  suppuration  in  the 
later  stages  of  the  pneumonia,  characteristic  of  the  pig,  and 
due  indirectly  to  the  irritation  of  perhaps  more  attenuated 
races  of  bacteria.  In  some  cases  there  are  extensive  hemor- 
rhages in  the  interlobular  connective  tissue.      (Fig.  9.) 

The  inflammation  of  the  pleura  frequently  extends  to  the 
pericardium.  This  membrane  is  opaque,  thickened,  and  its 
vessels  distended.  It  may  be  glued  to  the  contiguous  lobes  of 
the  lungs  and  covered  by  a  false  membrane,  smooth  or  rough- 
ened, which  extend  upon  the  large  vessels  emerging  at  its  base. 


58 


SWINE    PLAGUE 


Disease  of  the  digestive  tract  in  a  considerable  proportion 
of  animals  inoculated  with  swine-plague  cultures  consisted 
in'a  severe  catarrhal  inflammation  of  the  lining  membrane 
of  the  stomach.  The  hyperaemia  was  very  intense,  border- 
ing on  hemorrhage.  Occasionally  the  extension  of  the  peri- 
tonitis, produced  by  intra-abdominal  inoculation,  along  the 
mesentery  caUvSes  a  severe  inflammation  with  exudation  on  the 
mucosa  of  the  small  intestine.  A  case  is  reported  where  all 
the  Peyer's  patches  of  the  small  intestine  were  in  a  hyper- 
aemic,  and  partly  hemorrhagic  condition. 


Fig.  9.     Hemorrhage  into  interlobular  tissue  of  a  swine-plague  lung. 
— (a)  Hemorrhage,  [b)  hepalizcd  lobtiles 

In  the  naturally  contracted  disease  extensive  hyperaemia 
of  the  mucosa  of  the  large  intestine  bordering  on  a  hemorrhagic 
condition  has  been  observed.  In  other  cases  a  peculiar  croup- 
ous exudation  appeared,  which  seemingly  resulted  from  the 
effect  of  swine-plague  bacteria  in  the  large  intestine. 

The  production  of  intestinal  disease  by  swine-plague  bac- 
teria may  be  supposed  to  go  on  as  follows.  The  bacteria  first 
attack  the  lung  ti.ssue  and  there  produce  more  or  less  hepatiza- 
tion. The  blood  through  the  lungs  finds  its  path  partly  ob- 
structed. This  reacts  on  the  blood  in  the  right  side  of  the 
heart  and  the  venous  blood  entering  it.     Hence  there  may  be 


MORBID    ANATOMY  59 

more  or  less  stasis  of  blood  in  the  portal  circulation  which  in 
turn  impairs  the  digestive  functions  of  the  stomach.  The 
swine-plague  bacteria  in  the  lungs  in  the  later  stages  of  the 
pneumonia  may  be  coughed  up  in  the  contents  of  the  bronchial 
tubes,  swallowed  and  passed  through  the  impaired  stomach 
unharmed  into  the  intestines.  The  stagnation  of  the  feces  in 
the  large  intestine  furnishes  the  bacteria  an  opportunity  to 
cause  inflammation  with  exudation  of  the  mucous  membrane. 
The  tendency  of  swine-plague  bacteria  to  cause  fibrinous  in- 
flammatory deposits  on  serous  membranes  may  serve  to  explain 
such  action  on  mucous  membranes. 

There  is  general  congestion  with  resulting  degeneration 
of  the  parenchyma  of  the  spleen,  kidneys  and  liver  in  the  acute 
septicaemic  forms  of  the  disease.  In  these  cases  the  specific 
bacterium  is  easily  obtained  from  the  abdominal  organs.  In 
brief,  the  lesions  of  swine  plague  as  they  appear  in  various 
outbreaks  may  be  summarized  in  four  classes,  namely  : 

1.  Acute  septicaemia  form  in  which  the  lesions  are  char- 
acterized by  a  general  hyperaemic  condition  with  possibh' 
hemorrhages  on  the  serous  membranes  and  in  the  parenchyma- 
tous organs.      No  localized  lesions. 

2.  Cases  of  pneumonia  with  or  without  pleuritis.  The 
other  organs  remaining  normal  in  appearance. 

3.  Cases  where  either  in  addition  to,  or  po.ssibly  in  the 
absence  of,  the  lung  lesions  there  are  marked  anatomical 
changes  in  the  mucosa  of  the  dige.stive  tract  and  possibly  in 
the  lymphatic  glands. 

4.  Cases  of  mixed  infection,  especially  wdth  hog  cholera, 
where  in  addition  to  the  swine  plague  lesions  which  may  be 
more  or  less  modified,  there  are  those,  especially  of  the  digestive 
tract,  characteristic  of  the  accompanying  disease. 

In  order  to  present  as  clear  a  picture  as  possible  of  the 
findings  in  a  case  of  this  disease,  I  have  appended  the  pub- 
lished autopsy  notes  of  one  animal.  (Smith's  report  on  swine 
plague,  p.  62.) 

"Pig  died  yesterday,  put  on  ice.  Weighs  about  30  pounds.  Skin  on 
ventral  aspect  of  body  more  or  less  reddened  ;  over  the  sternum  a  few 
excoriations.     The  enlarged  inguinal  glands  show  as  lumps  under  the 


6o  SWINE    PI.AGUE 

skin.     On  section  they  present  a  mottled  gray  and  red  surface,  the  red 
limited  chiefly  to  the  cortex.     Oedema  of  the  subcutis  over  right  knee. 

False  membrane  covers  the  left  half  of  the  mass  of  intestines  and 
the  spleen  ;  consists  of  an  elastic,  rather  firm  yellowish  white  layer. 
Spleen  firmly  glued  to  the  surrounding  intestines,  slightly  enlarged, 
dark,  softened.  Liver  firm,  cuts  with  considerable  difficulty.  Kidneys 
in  condition  of  parenchymatous  degeneration.  One  hemorrhagic  spot  in 
medullary  portion  of  the  kidney.  Pelvis  contains  a  whitish  glairy 
liquid. 

Digestive  tract.  Two  superficial  necroses  on  the  inner  surface  of 
lower  lip  in  front,  one  on  the  upper  lip  and  on  edge  of  tongue  near  tip. 
Stomach  contains  a  little  deeply  bile-stained  fluid.  Mucosa  sprinkled 
with  red  spots  of  a  washed-out  appearance,  most  numerous  in  fundus 
and  near  pyloric  valve.  Hypersemia  of  duodenum  begins  sharply  at 
pyloric  valve.  From  the  opening  of  bile  duct  a  few  drops  of  thick  bile 
can  be  expressed.  Remainder  of  small  intestine  not  markedly  changed. 
The  Peyer's  patch  in  lower  ileum  has  some  of  its  follicles  enlarged  from 
which  caseous  masses  can  be  expressed. 

Large  intestine  contains  much  sand  and  gravel.  Mucosa  of  ciecum 
of  a  dark  slate  color.  The  summit  of  the  folds  of  a  purplish  hue.  Free 
edge  of  valve  bordered  by  a  thin  slough.  On  Peyer's  patch  near  valve 
areas  of  necrotic  tissue  of  a  yellowish  color,  resting  on  a  firm,  yellowish- 
white  base  three-sixteenths  of  an  inch  thick.  L'pper  colon  has  its 
mucosa  of  the  same  dark  slate  color,  merging  into  a  wine  red.  Two 
ulcers  one-eighth  of  an  inch  in  diameter  observed.  In  lower  colon  con- 
gestion slight  and  gradually  disappearing  towards  rectum.  A  small 
number  of  circular  whitish  erosions,  apparently  associated  with  the 
solitary  follicles. 

Thorax.  Of  the  left  lung,  the  ventral  and  cephalic  lobes  are  inter- 
spersed with  small  regions  of  collapse.  The  remainder  of  the  lobes  very 
emphysematous  and  hypersemic.  Of  the  right  lung,  the  anterior  half 
(i.  e.,  including  cephalic,  ventral,  and  adjacent  portion  of  principal 
lobes)  hepatized,  covered  by  a  thin  false  membrane,  gluing  the  various 
lobes  lightly  to  each  other  and  to  chest  wall.  The  diseased  lobes  show 
the  regular  mottling  in  the  upper,  dorsal  portion.  As  we  proceed 
towards  the  ventral  portion  the  mottling  is  less  distinct,  the  tissue  firmer 
and  interspersed  with  small,  irregular,  necrotic  foci.  The  smaller  bron- 
chi contain  a  thick,  whitish  pus.  In  ventral  lobe  a  portion  of  the  par- 
enchyma as  large  as  a  marble  completely  converted  into  a  grayish- 
yellow  hemogeneous  mass.  Of  the  principal  lobe  about  one-third  or 
one-fourth  hepatized.  The  mottling  of  surface  very  regular.  On  sec- 
tion grayish,  circumscribed  areas  one-half  an  inch  in  diameter  inter- 
spersed. Over  these  masses  the  pleura  is  converted  into  a  wrinkled, 
roughened,  hide-like  membrane. 

Trachea  and  bronchi  contain  small  quantities  of  foamy  liquid  inter- 
mingled with  yellowish  particles.  Bronchial  glands  barely  enlarged, 
firm  ;  some  lobules  pale,  others  reddened. 


MORBID    ANATOMY  6 1 

Bacteriological  notes.  At  the  autopsy  an  agar  tube  was  inoculated 
with  a  platinum  loop  lightly  rubbed  over  the  pleural  exudate.  On  the 
following  day  a  thin  grayish  growth  with  condensation  water  clouded. 
Examination  of  hanging  drop  and  stained  coverglass  preparations  shows 
only  swine-plague  germs. 

In  coverglass  preparations  of  hepatized  lung  tissue  a  large  number 
of  germs  resembling  swine-plague  bacteria  were  seen. 

With  a  bit  of  hepatized  lung  tissue,  a  rabbit  was  inoculated  subcu- 
taneously  at  2  p.  M.  The  rabbit  was  dead  next  morning  at  S  a.  m.,  i.  e., 
in  less  than  i8  hours.  In  spleen,  liver,  and  blood  preparations  numer- 
ous polar-stained  swine-plague  germs  present.  An  agar  culture  from 
heart's  blood  contained  only  swine-plague  germs. 

From  the  peritoneal  exudate  of  pig,  consisting  of  cells  and  fibrin 
and  numerous  bacteria  of  several  varieties,  two  agar  plate  cultures  were 
made.  On  Plate  A  one  large  colony  of  spore-bearing  bacilli  and  one 
small  colony  of  swine-plague  germs.  Plate  B,  completely  overgrown  by 
the  spore-bearing  bacillus. 

A  bouillon  culture  from  the  exudate  contains  streptococci  and 
swine-plague  bacteria.  Agar  plate  cultures  were  made  therefrom  and 
both  germs  isolated. 

At  the  same  time  a  large  rabbit  was  inoculated  subcutaneously  with 
a  bit  of  the  exudate  Dead  in  i8  hours.  Stained  coverglass  prepara- 
tions of  blood  from  heart,  spleen,  and  liver  tissue  show  polar-stained 
swine-plague  germs.  An  agar  culture  from  the  blood  contains  onh' 
swine-plague  germs. 

From  the  spleen,  after  thoroughly  scorching  through  the  exudate, 
two  agar  plate  cultures  and  a  bouillon  culture  were  made  with  bits  of 
spleen  pulp.     The  bouillon  culture  contained  only  swine-plague  germs. 

The  swine-plague  bacteria  were  thus  obtained  from  lungs,  pleura, 
spleen,  and  peritoneal  exudate,  while  hog-cholera  bacilli,  which  were 
looked  for  with  the  greatest  care,  could  not  be  found." 

^  50.  Differential  diagnosis.  In  sporadic  cases,  swine 
plague  is  to  be  differentiated  from  broncho-pneumonia  due 
to  other  causes  than  the  swine-plague  bacterium.  Pneumonia 
of  a  non-specific  nature  is  often  associated  with  deaths  due  to 
dietary  or  other  causes. 

In  epizootics  or  outbreaks  it  is  to  be  distinguished  from 
hog  cholera  when  there  is  accompanying  catarrhal  pneumonia. 
To  make  a  positive  diagno.sis  it  is  usually  necessary  to  depend 
upon  the  results  of  the  bacteriological  examination. 

Pneumonia  resulting  from  lung  worms,  (Strongylus  para- 
doxus) can  be  distinguished  by  a  careful  examination  of  the 
contents  of  the  bronchioles. 


62  SWINE   PLAGUE 

In  case  of  coexistence  of  hog  cholera  and  swine  plague  a 
bacteriological  examination  is  necessar}'  to  determine  the  pres- 
ence of  the  two  diseases  owing  to  the  possibility  of  an  accom- 
panying or  terminal  pneumonia  with  hog  cholera.  The  ques- 
tion has  arisen  as  to  whether  the  presence  of  B.  septicaeviiae 
hemorrhagicae  in  the  hepatized  lung  constitutes  a  diagnosis  of 
swine  plague.  As  understood  at  the  present  time  it  would 
seem  that  the  presence  of  this  species  of  bacteria  would  indi- 
cate the  nature  of  the  disease.  It  must  be  remembered,  how- 
ever, that  bacteria  not  readily  distinguishable  from  the  swine- 
plague  organism  exists  in  the  normal  upper  air  passages  from 
whence  it  could  be  brought  into  the  diseased  lung  and  in  such 
a  case  it  might  appear  as  a  secondary  element  only,  or  it  might 
have  been  primarily  the  cause  of  the  lesions.  It  is  not  im- 
probable that  epizootics  may  start  from  these  sporadic  cases, 
although  conclusive  proof  of  this  is  still  wanting.  It  seems, 
however,  that  the  presence  of  this  organism  in  the  lung  tissue 
of  a  sporadic  case  should  be  considered  in  the  light  of  the  dis- 
tribution of  these  organisms  and  not  necessarily  as  the  starting 
of  an  epizootic. 

§  51.  Prevention.  Recent  investigations  show  that  out- 
breaks of  swine  plague  are  much  more  extensive  than  hereto- 
fore supposed.  The  present  knowledge  of  this  disease  indi- 
cates, that  the  adoption  of  measures  for  its  prevention  is  quite 
as  important  as  for  hog  cholera.  In  general  the  measures  to 
be  adopted  and  followed,  and  the  rules  to  be  observed  in  the 
prevention  of  epizootic  swine  plague  are  practically  the  same  as 
those  for  the  prevention  of  hog  cholera.  It  will  be  seen 
from  the  comparison  of  the  two  species  of  bacteria  that  the 
bacillus  of  hog  cholera  is  a  more  hardy  organism  than  that  of 
swine  plague,  Thus  the  swine-plague  bacterium  is  destroyed 
more  rapidly  by  drying  and  will  live  a  much  shorter  time  in 
the  soil.  However,  the  channels  through  which  it  maj-  gain 
access  to  a  herd  are  practically  the  same,  and  every  precaution 
suggested  in  reference  to  hog  cholera,  is  applicable  to  swine 
plague.  It  is  believed  that  the  time  during  which  a  field,  hog 
yard  or  pen  should  be  kept  free  from  swine  after  the  appear- 
ance of  the  disease  can,  with   safety,  be   shorter  after  swine 


SWINE   PLAGUE  .         63 

plague  than  after  hog  cholera.  In  any  case  several  months 
should  elapse  before  the  yards  or  pens  are  reoccupied.  If  the 
disease  appears,  the  well  animals  should  be  promptly  separated 
from  the  sick  and  placed  in  suitable  pens  or  yards — protected 
against  subsequent  infections,  and  given  an  abundance  of 
wholesome  food  and  water.  It  is  well  to  remove  the  sick 
animals  to  other  pens.  The  thorough  disinfection  of  the  in- 
fected pens  should  be  insisted  upon  before  they  are  again 
occupied. 

§  52.     Specific   treatment.     For  a  number  of  years  in- 
vestigations have  almost  constantly  been  under  way  in   the 
United  States  Bureau  of  Animal   Industry,  for   tiie  purpose  of 
finding  some  method  by  which   this  disease  could  be  success- 
fully and  specifically   treated   when   introduced   into  a  herd. 
Drugs  and  medicines  have  been   tried,  preventive  inoculations 
and  injections  of  toxins  have  been  made.     The  serum  therapy 
which  has  afforded  relief  in  certain  other  diseases  has  been  and 
is  now  being  tested  with  somewhat  favorable  results,  yet  we  do 
not  see  that  a  specific  therapeutic  agent  has  been  demonstrated. 
In  view  of  this  fact,  it  becomes  necessary  to  apply  with  renewed 
zeal  our  present   knowledge   of  the  nature  of  the  malady  and 
endeavor  to  prevent  its  occurrence  or  reappearance  by  keeping 
the  animals  under  the  best  possible  conditions.     Prevention  of 
the  disease  seems  to  be  the  best  remedy. 

§  53.  Swine  plague  in  rabbits.  In  1894,  Smith  and 
Moore  described  the  appearance  of  the  effect  of  swine-plague 
bacteria  in  rabbits  and  also  the  effect  of  resistance  on  the  part 
of  the  rabbit  on  the  form  of  the  resulting  lesions.  As  this 
disease  is  caused  by  a  bacterium  belonging  to  the  septicaemia 
hemorrhagica  group,  it  seems  desirable  that  the  results  above 
referred  to  should  be  restated.  The  appended  paragraphs  are 
taken  from  the  report  of  these  investigations. 

"  Among  the  forms  of  disease  observed  after  the  sub- 
cutaneous inoculation  of  rabbits  with  swine-plague  bacteria 
from  different  sources  (epizootics)  are  the  following  : 

1.  SepticEemia. 

2.  Peritonitis. 

3.  Pleuritis  (usually  with  pericarditis). 


64  IN    RABBITS 

4.  Pleuritis  (usually  with  pericarditis)  and  peritonitis. 

5.  Local  lesion  only. 

In  the  septicaemia,  death  ensues  within  eighteen  to  twenty- 
four  hours.  The  local  lesion  produced  at  the  seat  of  inocula- 
tion is  slight.  Bacteria  are  abundant  in  the  parenchyma 
(blood  vessels)  of  the  various  organs.  In  the  form  character- 
ized by  peritonitis  death  ensues  in  three  to  seven  days.  The 
local  lesion,  which  in  all  these  forms  of  disease  increases  in  ex- 
tent with  the  prolongation  of  the  life  of  the  animal,  is  here 
characterized  b}'  more  or  less  suppurative  infiltration  of  the 
skin  and  the  subcutis.  The  peritonitis  in  its  earlier  stages  is 
characterized  by  punctiform  hemorrhages  on  the  caecum  and 
a  fibrinous  or  cellular  exudate.  It  always  contains  immense 
numbers  of  bacteria.  When  pleuritis  is  also  present  the  exu- 
date usually  involves  the  pericardium  as  well.  It  varies  in 
amount  according  to  the  duration  of  the  disease  and  is  essen- 
tially the  same  as  the  peritoneal  exudate. 

The  form  characterized  by  pleuritis  and  pericarditis  with- 
out peritonitis  is  interesting  in  so  far  as  the  seat  of  inoculation 
does  not  explain  the  localization,  for,  in  every  case,  the  inocu- 
lation was  made  in  the  region  of  the  abdomen.  The  lungs 
may  become  hepatized  secondarily  through  invasion  from  the 
pleura  if  the  animal  lives  long  enough. 

Lastly,  the  form  of  disease  in  which  the  only  localization 
is  a  ver3'  extensive  suppurative  infiltration  associated  with 
hemorrhage  and  oedema  of  the  subcutaneous  tissue  is  not 
common. 

It  should  be  stated  that  the  cultures  from  the  same  out- 
break continued  to  produce  the  same  form  of  disease  in  rabbits 
until  modified  by  age.  The  maintenance  of  a  certain  uniform 
virulence  for  j'ears  is  well  exemplified  by  a  variet}'  isolated 
in  the  summer  of  1890.  This  variety  was  fatal  to  rabbits 
within  twenty  hours  when  first  isolated,  and  this  degree  of 
virulence  has  maintained  itself  up  to  the  present,  a  period  of 
nearly  four  years." 

§  54.  Modifications  of  the  septicaemia  type  by  in- 
creasing the  resistance  of  rabbits.  By  the  infection  of  steril- 
ized cultures  which  increase  the  resistance  of  rabbits,  Smith  and 


SWINE   PI.AGUE  65 

Moore  were  able  to  produce  nearly  all  the  pathological  variations 
which  follow  the  inoculation  of  natural  races  of  swine-plague 
bacteria  as  isolated  from  outbreaks.  This  modification  of  the 
septicaemia  type  is  not  fortuitous,  for  among  the  large  number 
of  rabbits  inoculated  during  the  past  three  and  one-half  years 
with  the  culture  employed,  none  have  survived  twenty  to 
twenty-four  hours.  Whenever  the  course  of  the  inoculation 
disease  in  rabbits  departed  from  this  rapidly  fatal  type,  it  was 
due  to  some  preliminary  treatment  of  the  rabbit. 

'  'The  degree  of  resistance  determined  quite  regularly  though 
not  invariably  the  form  of  the  disease.  This  degree  was  meas- 
ured by  the  relative  quantity  of  the  protective  material  (steril- 
ized cultures,  sterilized  blood,  and  blood  serum)  injected.  The 
grades  of  disease  induced  range  themselves  in  the  following 
order  : 

1.  No  resistance — acute  septicaemia. 

2.  Slight  resistance — peritonitis. 

3.  Increased  resistance — pleuritis  and  pericarditis  with  or  with- 

out secondary  pneumonia. 

4.  Higher  degree  of  resistance— pleuritis  and  peritonitis. 

5.  Still  greater  resistance— irregular  lesions  in  the  form  of  ab- 

scesses, subcutaneous  and  subperitoneal. 

6.  Nearly   complete  immunity.     Very   slight   reaction    at   the 

point  of  inoculation. 

Most  of  the  cases  cited  below  as  illustrating  these  modified 
forms  of  the  septicaemia  type  belong  to  the  series  of  immuniz- 
ing experiments  of  the  preceding  article.  To  this  the  reader 
is  referred  for  additional  illustrations. 

First  degree  of  resistayice— peritonitis. — Rabbit  No.  12  re- 
ceived 7  cc.  of  bouillon  culture  of  swine-plague  bacteria  steril- 
ized by  heat.  Subsequently  with  a  control  rabbit  it  was  inocu- 
lated with  a  minute  dose  of  swine-plague  bacteria  under  the 
skin.  The  control  died  within  eighteen  hours,  the  treated 
rabbit  in  three  days.  The  macroscopic  changes  were  limited 
to  the  point  of  inoculation  and  the  peritoneum.  At  the  former 
there  was  a  purulent  infiltration  of  the  subcutis,  1.5  cm.  in 
diameter,  with  dilatation  of  surrounding  blood  vessels.  The 
peritonitis  was  characterized  by  an  exudate  of  a  slightly  viscid 
character  covering  liver,  spleen,  and  caecum,  and  made  up  of 
fibrin,  leucocytes,  and  immense  numbers  of  bacteria. 


66  IN    RABBITS 

Second  degree  of  resistance — plcicritis  and  pericarditis .  — Rab- 
bit No.  38  was  treated  before  inoculation  with  4.5  cc.  of  a  steril- 
ized suspension  of  agar  cultures  of  swine-plague  bacteria  in  5 
doses.  Together  with  a  control  rabbit,  it  received  under  the 
skin  the  equivalent  of  o.ooi  cc.  of  a  fresh  bouillon  culture  of 
swine-plague  bacteria.  The  control  died  in  twenty  hours.  The 
treated  rabbit  died  six  days  after  inoculation.  At  the  point  of 
inoculation  there  was  a  purulent  infiltration  of  the  subcutis  3 
cm.  in  diameter.  The  abdomen  and  abdominal  viscera  were 
free  from  macroscopic  changes.  In  the  thorax,  the  pleural 
cavity  was  lined  with  a  grayish,  friable  exudate  consisting  of 
round  cells  and  bacteria.  Lungs  hyperaemic  and  only  partly 
collapsed.     Pericardium  also  covered  with  a  slight  exudate. 

Third  degree  of  resistance — pleuritis  {^pericarditis^  and peri- 
tonitis. — Rabbit  No.  15  received  in  the  ear  vein  12  cc.  of  a  ster- 
ilized bouillon  culture  of  swine-plague  bacteria.  It  was  inocu- 
lated subcutaneously  with  virulent  swine-plague  bacteria  May 
26,  and  died  June  3,  eight  days  later.  The  control  rabbit  died 
within  eighteen  hours.    The  following  changes  were  observed  : 

A  purulent  infiltration  into  the  subcutaneous  tissue  at  the  point  of 
inoculation  extending  over  an  area  6  cm.  in  diameter.  The  superficial 
layer  of  the  subjacent  muscle  discolored.  Surrounding  the  area  of  infil- 
tration the  blood  vefesels  were  injected.  The  caecum  and  liver  were  cov- 
ered with  a  very  thin  grayish  exudate,  which  also  appeared  on  and  be- 
tween the  coils  of  the  intestine.     Spleen  not  enlarged. 

The  right  lung  and  chest  wall  covered  with  a  thin  grayish  exudate. 
In  the  cephalic  lobe,  two  small  areas  of  consolidation  ;  principal  lobe 
hyperaemic.  The  left  pleural  cavity  lined  with  a  quite  thick  membran- 
ous exudate,  which  covered  the  entire  surface  of  the  lung.  On  the  dor- 
sal surface  of  the  principal  lobe  a  mass  of  lung  tissue  2  cm.  in  diameter, 
firm  and  of  a  yellowish-gray  color.  The  remaining  portion  of  the  prin- 
cipal lobe  hyperaemic  ;  cephalic  lobe  in  a  state  of  collapse. 

Pericardium  covered  with  a  thin  cellular  exudate. 

Higher  degrees  of  resistance. — None  of  the  treated  animals 
which  have  come  under  our  observation,  have  succumbed  to  a 
mere  extension  of  the  lesion  produced  at  the  point  of  inocula- 
tion as  is  occasionally  observed  after  inoculation  with  certain 
varieties  of  swine-plague  bacteria  found  in  nature.  There  have 
been  noticed,  however,  certain  peculiar  localizations  resem- 
bling those  produced  in   the  subctitis  after  inoculation,  and  in 


SWINE   PLAGUE  67 

a  few  cases  the  local  lesion  persisted  a  considerable  length  of 
time.  It  was  quite  severe  in  all  fatal  cases  in  which  the  disease 
was  prolonged  several  weeks  after  inoculation,  although  the 
real  cause  of  death  was  due  in  all  such  cases  to  localizations  on 
one  or  more  of  the  serous  membranes.  The  peculiar  forms  of 
disease  may  be  grouped  as  follows  : 

(a)  Persistence  of  local  lesions. — Rabbit  No.  50  received  in  the  ab- 
dominal cavity  3.5  cc.  of  the  sterilized  suspension  of  agar  cultures  in  3 
doses.  It  was  subsequently  inoculated  beneath  the  skin  vyith  o.ooi  cc. 
of  a  bouillon  culture  of  swine-plague  bacteria  which  produced  a  large 
local  swelling.  On  February  25,  1S92,  nearly  eight  months  after  its 
inoculation  it  was  chloroformed.  The  only  lesion  found  was  in  the 
subcutaneous  tissue.  At  the  point  of  inoculation  the  skin  was  sloughed 
over  an  area  of  3  cm.  in  diameter.  This  denuded  surface  was  covered 
with  a  thick  scab.  The  subcutis  beneath  the  scab  and  surrounding  the 
ulcer  was  infiltrated  with  pus.  A  stained  cover-glass  preparation  showed 
swine-plague  bacteria.     No  other  lesions  were  found. 

{b)  Sub-peritoneal  abscess. — Rabbit  No.  16  was  injected  intraven- 
ously with  16  cc  of  sterilized  bouillon  cultures  of  swine-plague  bacteria. 
After  some  days  it  was  inoculated  beneath  the  skin  with  o.ooi  cc.  of  a 
fresh  bouillon  culture  of  virulent  swine-plague  bacteria.  The  control 
rabbit  died  within  twenty  hours.  Rabbit  No.  16  showed  no  ill  effect 
from  the  inoculation  for  several  months  when  it  was  noticed  that  it  was 
becoming  emaciated.  It  died  June  11,  1892,  one  year  and  six  days  after 
its  inoculation  with  an  enormous  subperitoneal  tumor. 

(c)  Multiple  abscesses  under  the  skin. — Rabbit  No.  439  received  into 
the  ear  vein  in  three  injections  4  cc.  of  sterilized  blood  from  a  swine 
plague  rabbit.  Later  it  was  inoculated  subcutaneously  with  0.001  cc.  of 
a  bouillon  culture  of  virulent  swine-plague  bacteria.  The  control  rabbit 
died  within  twenty  hours.  Two  months  after  the  inoculation  it  was 
noticed  that  this  rabbit  with  others  was  suffering  from  a  large  number 
of  subcutaneous  abscesses. " 

REFERENCES. 

1.  DE  ScHWEiNiTz.  Serum  therapy.  Proceedings  Society  for  the 
Promotion  of  Agricultural  Science.     1896.     p.  47. 

2.  DE  ScHWEiNiTZ.  The  serum  treatment  of  swine  plague  and 
hog  cholera.  Bulletin  No.  23.    U.  S.  Bureau  of  Animal  Industry.    1S99. 

3.  LoEFFLER.    Arbeiten  a.  d.  Kaiserlichen  Gestmdheitsamte.    Bd.  I 

(1885)  S.  5t. 

4.  MooRE.  Pathogenic  and  toxicogenic  bacteria  in  the  upper  air 
passages  of  domesticated  animals.  Bulletin  No.  3.  U.  S.  Bureau  of 
Ani)nal  Industry.     1893.  ' 

5.  Moore.  Concerning  the  nature  of  infectious  swine  diseases  in 
the  State  of  New  York  with  practical  suggestions  for  their  prevention 
and  treatment.  Report  of  the  New  York  State  Commissioner  of  Agri- 
culture.    1897. 


68  HEMORRHAGIC   SEPTICAEMIA 

6.  Smith.  Preliminary  investigations  concerning  infectious  pneu- 
monia in  swine  (Swine  plague).  Annual  Report  Bureau  of  Animal 
Industry  U.  S.  Dept.  of  Agriculture.     iS86.     p.  76. 

7.  Smith.  Special  report  on  swine  plague.  Bureatc  of  Animal 
Industry.     U.  S.  Dept.  of  Agriculture.     1S91. 

8.  Smith  AND  Moore     Experiments  on  the  production  of  immunity 
in  rabbits  and  guinea  pigs  with  reference  to  hog  cholera  and  swine  plague 
bacteria.     Bulletin  No.  6.     Bureau  of  Animal  Industry,  U.  S.  Dept.  of 
Agriculture.     1894.     p.  65. 

9.  Welch  and  Clements.  Remarks  on  hog  cholera  and  swine 
plague.     First  International  Congress  of  America.     Chicago.     1893. 


HEMORRHAGIC  SEPTICAEMIA  IN  CATTLE. 

§  55.  Characterization.  Hemorrhagic  septicaemia  in 
cattle  is  determined  by  an  acute  attack  usually  running  a 
rapid  course  and  terminating  fatally.  The  lesions  consist 
largely  of  hemorrhagic  areas  more  or  less  widely  distributed 
throughout  the  body  and  due  to  the  presence  of  a  specific 
microorganism . 

ij  56.  History.  In  1879,  Bollinger  described  under  the 
name  of  Wild  iind  Rinderseiiche  an  epizootic  disease  which 
killed  a  large  number  of  wild  boars  and  deer  in  the  Royal 
game  preserves  of  Munich.  After  the  disease  in  these  animals 
had  died  out,  the  domestic  cattle  in  the  neighborhood  began 
to  die  of  the  same  or  a  very  similar  affection.  He  reports  it  to 
be  sudden  in  its  onset  and  rapidly  fatal  in  its  course,  with  a 
mortality  of  90  per  cent.  Death  occurred  in  from  12  hours  to  a 
few  days  after  the  first  appearance  of  symptoms. 

Two  forms  are  described,  (i)  an  exanthematous  and  (2)  a 
pectoral.  The  post-mortems  showed  in  the  exanthematous 
form  large  and  small  hemorrhages  disseminated  throughout  the 
muscles  and  viscera.  The  intestines  always  exhibited  large 
numbers  of  ecchj-motic  areas,  while  the  submucous  tissue  was 
infiltrated  with  a  serous  exudate.  L,arge  hemorrhagic  tumors 
infiltrated  with  serum  were  abundant  in  the  subcutaneous  tissue 
and  penetrated  the  muscles.  The  mucous  membranes  of  the 
tongue,  larynx  and  pharynx  and  the  lymphatic  glands  of  these 
regions  were  swollen  and  infiltrated  with  more  or  less  bloody 
serum.    In  the  pectoral  form,  a  hemorrhagic  lobular  pneumonia. 


HISTORY  69 

with  considerable  infiltration  into  the  interlobular  tissue  of  a 
serofibrinous  exudate  was  present.  The  pleura  was  infiltrated 
and  inflamed  and  covered  with  a  fibrinous  exudate.  The 
pleural  cavities  contained  from  two  to  twenty-five  litres  of 
liquid.  At  the  same  time  there  existed  a  certain  degree  of 
hemorrhagic  enteritis  and  the  wideh*  disseminated  hemor- 
rhagic lesions  common  to  the  preceding  form. 

In  1885,  Kitt  studied  an  epizootic  disease  in  cattle  and 
swine  in  Sincbach.  From  this  disease  he  isolated  a  short, 
polar  staining,  non-motile,  rod  shaped  organism,  fatal  to  cattle, 
horses,  pigs,  sheep,  goats,  dogs  and  rabbits.  In  the  fol 
lowing  year  Oreste  and  Armanni  reported  a  destructive  dis- 
ease of  young  buffaloes  in  Italy  with  symptoms  and  lesions 
similar  to  those  reported  by  Bollinger  and  Kitt.  This  dis- 
ease had  been  known  in  Italy  for  a  century  or  more  where 
in  certain  districts  it  is  reported  to  have  recurred  with  great 
regularity  destroying  both  old  and  young  animals.  In  the 
same  year  (18S6)  Poels  described  a  septic  pleuro-pneumonia  in 
calves  which  prevailed  in  the  vicinity  of  Rotterdam.  It  was 
of  a  septicaemia  nature.  From  the  organs  he  obtained  an 
organism  belonging  to  the  Bacillus  scpticaemiae  hcniorrhagicae 
group  of  bacteria.  In  1889,  Jensen  described  a  similar  disease 
affecting  calves  in  Jutland.  In  18S9,  Piot  reported  the 
presence  of  "  barbone  "  in  the  buffaloes  and  domestic  cattle  in 
Egypt.  In  some  districts  40  per  cent,  of  the  horned  cattle  are 
said  to  have  died  in  a  single  year.  It  is  reported  as  being 
more  prevalent  in  the  wet  season. 

In  1S90,  Van  Ecke  described  a  hemorrhagic  septicaemia 
in  cattle  in  Dutch  India,  particularly  in  Java,  the  lesions  of 
which  were  similar  to  those  first  described  by  Bollinger.  The 
specific  organism  was  virulent  for  rabbits,  mice,  turtle  doves, 
calves,  horses  and  swine  ;  sheep  and  asses  were  almost  im- 
mune. In  the  following  year  Galtier  described  the  same  dis- 
ease imported  from  Algiers  to  Lyons.  A  number  of  other  in- 
vestigators, among  whom  may  be  mentioned  Reischig,  Bon- 
garts,  Jakobi,  Buch,  Janson,  Guillebeau  and  Hess,  Von  Ratz, 
Fischer,  Lignieres  and  others,  have  studied  and  reported  cases 
of  this  disease.    In  1890,  Nocard  isolated  from  cases  of  broncho- 


7©  SEPTICAEMIA    HEMORRHAGICA 

pneumonia  in  American  cattle  landed  at  La  Villette,  France,  an 
organism  similar  to  that  described  as  the  cause  of  septicaemia 
hemorrhagica.  In  1896,  Smith  called  attention  to  a  similar  or- 
ganism which  he  found  in  cases  of  sporadic  pneumonia  in  cattle  ; 
he  does  not  think,  however,  that  this  organism  was  primarily 
the  cause  of  the  disease,  giving  it  a  secondary  place  in  the  eti- 
olog3\  As  early  as  1891,  Smith  published  the  discovery  of  the 
presence  of  an  organism  morphologically  and  in  its  cultural 
characters  identical  with  that  of  swine  plague  in  the  upper  air 
passages  of  healthy  swine.  The  same  year  Moore  reported  the 
presence  of  a  like  organism  in  the  upper  air  passages  of  cattle, 
horses,  sheep,  dogs,  and  cats.  The  following  year,  Fiocca  de- 
.scribed  a  pathogenic  bacillus  resembling  that  of  rabbit  septi- 
caemia in  the  saliva  of  cats  and  dogs. 

Hueppe  proposed  the  name  Bacillus  septicaeviiae  hcmor- 
rhagicae  for  this  group  of  organisms  and  septicaemia  hemor- 
rhagica for  the  disease  they  produce.  While  there  may  be 
objections  to  this  unifying  name,  there  seems  to  be  no  serious 
reason  for  not  accepting  it  as  a  working  hj'pothesis.  In  1898, 
Fennemore  described  under  the  name  of  "Wild  and  Cattle 
Disease"  a  malady  occurring  in  Eastern  Tennessee.  Its  seri- 
ous nature  caused  an  investigation  to  be  made  by  the  Tennessee 
Agricultural  Experiment  Station  in  which  it  was  recognized 
by  Norgaard,  wdio  assisted  in  this  investigation,  as  the  same 
disease  described  by  Bollinger  in  1S78.  Fennemore  states  that 
it  has  occurred  to  a  considerable  extent  in  his  practice.  In 
1 90 1,  it  was  carefully  studied  by  Wilson  and  Brimhall  for  the 
Minnesota  State  Board  of  Health.  They  report  60  cases  of  this 
affection  which  they  have  examined  in  cattle  in  the  state  of 
Minnesota.  It  is  from  their  report  that  we  draw  very  largely 
for  the  symptoms  and  morbid  anatomy  of  this  disease  in  cattle. 

§  57.  Geographical  distribution.  It  will  be  seen  from 
the  history  that  this  disease  is  a  wide  spread  malady  occurring 
in  nearly  ever\'  country.  It  appears  to  be  quite  prevalent  in 
the  western  part  of  the  Mississippi  valley. 

§  58.  Etiology.  Septicaemia  hemorrhagica  in  cattle  is 
caused  b}^  an  organism  belonging  to  the  group  of  bacteria 
designated  by  Hiippe  as  the  hemorrhagic  septicaemia  group 


ETIOLOGY  7 1 

and  specificalh-  named  as  Bacillus  boviseptiais  hy  Krnse.  This 
according  to  Migula's  classification,  should  be  Bacterium 
bovisepticiun.  A  brief  description  of  the  organism  as  given  by 
Wilson  and  Brimhall  is  appended. 

"  The  organism  has  a  strong  tendency  to  show  polar  staining  in  tis- 
sues and  to  form  chains  of  much  shortened  individuals  in  liquid  media 
which  causes  it  to  be  mistaken  in  examinations  of  a  single  specimen  for 
a  diplococcus  or  a  streptococcus.  Sometimes  in  cover-glass  preparations 
from  solid  organs  and  very  frequently  in  those  from  body  fluids  and 
liquid  cultures,  the  bacteria  were  found  in  chains  of  three  to  twelve  indi- 
viduals. In  cover-glass  preparations  the  bacteria  are  from  0.6// to  0.8// 
broad  and  from  i.o  to  1.5'/  in  length.  In  tissues  which  have  been  fixed 
in  96  per  cent,  alcohol,  they  are  somewhat  smaller.  In  cultures,  especially 
in  fluid  media,  they  are  apt  to  be  much  smaller  and  approach  diplococci 
in  appearance.  The  ends  are  rounded.  In  stained  preparations  directly 
from  the  tissues  most  of  the  bacteria  have  the  ends  intensely  stained 
and  the  central  portion  but  faintlj-  so.  In  some  chains  in  rapidly  grow- 
ing broth  cultures  this  is  not  the  case,  many  of  the  individual  bacteria 
being  evenly  stained  throughout  and  somewhat  pointed  at  the  ends. 
They  do  not  retain  the  stain  by  Gram's  method.  The  organism  is  non- 
motile.  It  is  aerobic,  but  prefers  the  depths  rather  than  the  surfaces  of 
the  media.  It  grows  best  at  the  body  temperature  and  more  slowly  at 
room  temperature.  In  plain  and  dextrose  broth  a  heavy  growth  appears 
in  24  hours.  In  Dunham's  solution  a  small  amount  of  indol  is  formed 
in  48  hours.  No  coagulation  of  milk.  On  Lofflers  blood  serum,  direct 
from  the  diseased  tissues,  it  failed  to  grow  well.  On  potato  no  appreci- 
able growth  has  been  obtained.  In  gelatin  plates  small,  granular  white  to 
slightly  yellowish  colonies  appear  after  48  hours.  In  gelatin  stab  cul- 
tures a  light  growth  occurs  on  the  surface,  while  along  the  needle  tract 
numerous  colonies  like  those  in  the  deep  portions  of  the  plate  cultures 
develop.  The  bacteria  are  destroyed  in  fluids  at  58°  C.  in  7  or  8  minutes, 
by  I  to  5,000  mercuric  choloride  in  i  minute,  and  by  a  solution  of  lime 
water  as  weak  as  0.04  per  cent,  almost  immediately." 

§  59.  Symptoms  There  is  little  opportunity  to  deter- 
mine the  sjmiptoms.  The  animals  observed  at  the  onset  of  the 
disease  by  Wilson  and  Brimhall,  appeared  dumpish  and  out  of 
sorts.  There  is  sudden  stopping  of  the  milk  secretion  in  milch 
cows.  As  a  rule  the  affected  animals  refused  food.  Of  the  few 
that  make  an  attempt  to  eat,  those  with  affected  throats  were 
unable  to  swallow  except  with  much  difficulty.  These  cases 
also  breathed  very  heavih'.  The  animals  showed  marked  disin- 
clination to  move  and  when  incited  to  do  so,  exhibited  stiffness, 


72  SEPTICAEMIA    HEMORRHAGICA 

and  in  some  instances  actual  lameness.  Some  of  the  animals 
dropped  to  the  ground  and  died  in  a  short  time,  apparent!}' 
without  pain.  Others  were  down  when  first  observed  to  be 
sick  and  lived  for  several  hours  in  great  pain  as  indicated  b}' 
groans,  and  spasms  of  the  muscles.  The  paroxysms  of  pain 
were  apparently  intermittent.  There  was  extremely  rapid  loss 
of  flesh  in  the  animals  that  were  sick  more  than  one  daj-. 

Opportunities  for  the  accurate  determination  of  tempera- 
ture at  the  beginning  of  the  disease  were  very  few.  It  appears 
that  an  initial  temperature  of  105.6°  F.  was  present  followed 
by  a  rapid  decline.  Painful  oedematous  swellings  about  the 
legs,  shoulders  and  under  the  throat  were  noted  as  early  symp- 
toms. The  intestinal  discharges  were  often  streaked  with 
blood.  In  other  cases  the  feces  were  black,  tarry  or  of  a  bloody, 
serous  nature..  Bloody  urine  and  a  bloody  serous  discharge 
from  the  nose  were  present  in  some  of  the  cases.  The  vaginal 
and  rectal  mucous  membranes  were  intensely  congested. 

The  marked  swellings  of  the  face,  stomatitis,  glossitis,  and 
convulsive  movements  of  the  jaws  in  the  pneumonic  form  of 
the  disease  described  by  European  writers,  more  especially 
Bollinger,  were  not  observed  by  Wilson  and  Brimhall  in  an}^ 
of  the  recent  cases. 

§  60.  Morbid  anatomy.  The  characteristic  lesions  of 
the  disease  are  widely  distributed  areas  of  hemorrhage,  vary- 
ing in  size  from  a  pin  point  to  several  centimeters  in  diameter. 
They  vary  in  color  from  light  red  to  almost  black.  They  are 
frequently  accompanied  with  a  sero-fibrinous  exudate,  usually 
yellow,  but  occasionally  dark  red  in  color.  The  hemorrhagic 
areas  in  the  animals  just  dead  are  not  so  dark  as  those  in 
animals  that  have  been  dead  for  some  hours.  The  large  areas, 
some  centimeters  in  diameter,  are  apparently  due,  in  some 
instances,  to  single  hemorrhages  infiltrating  an  extensive  mass 
of  tissue,  and  in  others  to  a  number  of  minute  hemorrhages 
closely  placed  and  partially  coalescing.  Gas  is  not  present  in 
the  subcutaneous  connective  tissue  except  cases  where  exten- 
sive post-mortem  changes  have  occurred. 

There  is  excessive  fullness  of  the  vessels  of  the  subcu- 
taneous  connective   tissue  in   the  acute   cases,    especialh*    in 


MORBID    ANATOMY  73 

those  animals  which  are  not  killed  by  bleeding.  In  animals 
which  live  until  emaciation  is  marked,  there  is  no  engorge- 
ment of  the  vessels. 

All  cases  show  some  hemorrhagic  areas  in  the  subcu- 
taneous tissue,  though  the  number  and  size  of  these  vary 
greatly  in  the  different  cases.  Some  animals  show  not  over  a 
dozen  areas  between  two  and  three  centimeters  in  diameter, 
though  many  minute  ones  are  present.  In  other  animals,  on 
removing  the  skin,  hemorrhagic  areas  are  found  in  great  num- 
bers and  so  extensive  that  a  large  fraction,  possibly  one-eighth, 
of  the  body  surface  appears  to  be  involved.  The  large  hemor- 
rhages in  the  subcutaneous  connective  tissue  appear  to  be  of 
the  composite  type  noted  above. 

The  location  of  the  superficial  lesions  varies  in  different 
animals.  In  most  cases  the  parts  about  the  shoulder  are  most 
affected, — in  some  the  throat,  and  in  others  the  digital  region. 
A  few  animals  show  marked  lesions  in  the  gluteal  and  inguinal 
regions. 

At  first  sight  the  muscle  tissue  in  some  cases  seems  to  be 
much  involved.  A  closer  examination,  however,  usually 
shows  that  while  some  of  the  minute  hemorrhages  are  in  the 
muscle  proper,  the  larger  ones  are  in  the  intermuscular  con- 
nective tissue.  The}'  are  usually  accompanied  by  a  consider- 
able quantity  of  yellowish  or  blood  stained  serous  exudate. 
The  intermu.scular  conneciive  tissue  appears  to  be  quite  as 
much  involved  as  the  subcutaneous  connective  tissue. 

The  lymphatic  glands  are  frequently,  though  not  uni- 
formly nor  constantly  enlarged.  Those  that  are  enlarged  are 
oedematous  and  often  hemorrhagic.  The  most  constantly  and 
seriously  affected  are  the  cervical  and  prescapular. 

The  nasal  mucous  membrane  in  some  cases  is  congested, 
and  a  bloody  serous  discharge  from  the  nostrils  is  present  in 
a  few  cases.  The  tissues  around  the  larynx  are  hemorrhagic 
and  infiltrated  with  blood  stained  serum.  The  mucous  mem- 
branes of  the  larynx  and  trachea  are  more  or  less  congested 
and  covered  with  a  frothy  mucus,  sometimes  streaked  with 
blood.  In  some  instances  no  lesions  are  observable  in  the 
larynx  and    trachea.     The  lungs    are   in  general  almost  free 


74  SEPTICAEMIA    HEMORRHAGICA 

from  evidence  of  disease.  A  few  showed  a  small  number  of 
hemorrhagic  areas,  pyramidal  in  shape  with  their  bases  on  the 
pleura.  In  most  cases  the  parietal  pleura  is  studded  with 
small  hemorrhages.  The  diaphragm  sometimes  contains  very 
large  hemorrhagic  areas. 

The  pericardial  sac  usually  shows  small,  sometimes  very 
numerous  hemorrhages  in  the  walls,  and  in  many  instances 
contains  a  blood  stained  serum. 

The  heart  walls,  with  but  few  exceptions,  contain  large 
and  small  hemorrhages.  These  sometimes  extend  deep  into 
the  muscle.  Similar  areas  of  hemorrhage  are  also  visible  in  the 
endocardium.  The  heart  contains  blood  clots,  post-mortem  in 
formation. 

The  blood,  in  animals  just  dead,  is  somewhat  lighter  than 
normal  in  color.  When  post-mortem  changes  set  in,  the  blood 
is  darker  in  color,  but  reddens  on  exposure  to  the  air. 

The  spleen  shows  on  its  surface  a  few  small  hemorrhagic 
areas.  It  is  usually  normal  in  size,  color  and  consistency, 
except  where  post-mortem  changes  have  taken  place. 

Stomatitis  and  glossitis  are  rarely  observed.  The  pharynx 
is  usually  congested. 

The  stomach  walls  contain  few  or  many  hemorrhagic 
areas.  These  are  sometimes  extremely  large,  especially  on 
the  third  stomach .  As  a  rule  the  larger  hemorrhages  penetrate 
the  entire  thickness  of  the  walls.  The  smaller  ones  are  con- 
fined to  the  subserous  or  mucous  coats.  The  stomach  contents 
are  apparently  normal. 

The  intestinal  walls  are  constantly  affected.  Hemorrhagic 
areas  involving  all  the  coats  are  frequently  present.  Smaller 
ones,  visible  only  from  the  inner  or  outer  surface,  are  always 
present.  General  enteritis  and  peritonitis  are  occasionally  ob- 
served.     Localized  enteritis  is  frequent. 

The  bowel  contents  are  in  some  cases  dark  and  tarry  ;  in 
others  the  feces  are  apparently  normal  in  color  and  consistency 
but  streaked  with  bloody  mucus. 

The  kidneys  are  usually  but  slightly  affected.  When  le- 
sions are  present  they  are  but  pin  point  in  size  and  mostly 
confined  to  the  cortical  substance,  though   a  few  are  found  in 


MORBID    ANATOMY  75 

the  walls  of  the  pelvis   and   ureters.     The  urine  is  bloody  in 
some  instances. 

The  vaginal  mucus  membrane  is  congested  in  many  cases. 
Wilson  and  Brimhall  saw  one  animal  that  was  four  months 
pregnant,  which  exhibited  small  areas  of  hemorrhage  in  the 
placental  membranes. 

The  udder  is  congested  in  some  cases,  in  one  instance  it 
appeared  as  one  mass  of  blood. 

The  central  nervous  system  was  examined  in  but  three 
cases.  The  first  two  showed  hemorrhages  in  the  dura.  An 
examination  of  a  small  portion  of  the  cord  showed  no  lesions. 
Two  cases  showed  hemorrhages  in  all  of  the  joint  surfaces. 

Portions  of  the  subcutaneous  tissue,  skeletal  muscles,  lym- 
phatic glands,  lung,  heart  wall,  stomach  wall,  and  spleen 
were  fixed  in  95  per  cent,  alcohol  and  in  4  per  cent,  formal- 
dehyde solution  and  stained  by  various  methods  by  Wilson  and 
Brimhall.  In  general,  the  lesions  found  were  enormous  ex- 
travasations of  blood,  some  recent  and  some  showing  coagula- 
tion of  fibrin.  In  the  areas  of  less  recent  hemorrhage,  the  sur- 
rounding tissues  showed  varying  degrees  of  ordinary  coagula- 
tion necrosis.  This  was  particularly  marked  in  the  affected 
muscles,  lymph  glands,  and  portions  of  the  lungs.  In  the  bor- 
ders of  such  necrosed  areas  leucocytic  infiltration  was  not  in- 
frequent. In  the  spleen  in  which  the  hemorrhagic  areas  were 
neither  numerous  nor  large  ;  there  was  in  some  instances,  an 
apparent  destruction  or  shrinkage  of  the  parenchyma. 

A  very  important  feature  in  this  disease  has  been  brought 
out,  namely,  that  is  it  necessary,  in  order  to  obtain  cultures  of 
the  bacterium  producing  it,  that  the  media  should  be  inocu- 
lated at  once.  It  is  evident  from  the  literature  that  with  this 
precaution  cultures  should  invariabh-  be  obtained.  The  writer 
had  occasion  to  investigate  an  outbreak  of  disease  of  consider- 
able proportions  in  Central  New  York  where  the  lesions  cor- 
responded exactly  with  those  more  recently  described  by  Wil. 
son  and  Brimhall.  Allthough  a  very  large  number  of  cover- 
glass  preparations  from  the  blood  and  different  tissues  were 
made  and  stained  by  various  solutions  and  methods,  and  many 
tubes  of  bouillon,  agar  and  gelatin  were  inoculated,  bacteria 
were  not  found  in  the  tissues  of  any  of  the  animals  examined. 


76  SEPTIACEMIA    HEMORRHAGICA 

§  6i.  Differential  diagnosis.  Septicaemia  hemorrha- 
gica in  cattle  must  be  differentiated  from  anthrax,  sympto- 
matic anthrax,  and  the  affection  known  as  "corn  stalk  dis- 
ease." Death  from  this  disease  must  also  be  distinguished 
from  those  due  to  certain  accidental  causes,  poisoning,  or  the 
-effect  of  over  eating  of  grain  or  green  fodder  (hoven).  The 
suddenness  with  which  the  animals  may  die  from  all  of  these 
causes  renders  the  symptoms,  should  they  be  observed,  of  very 
little  value  in  making  a  diagnosis.  It  is  necessary,  therefore, 
that  in  all  cases,  especially  with  the  first  animals  to  die  that 
-careful  post-mortem  and  bacteriological  examinations  should 
be  made. 

In  case  of  septicaemia  hemorrhagica,  the  cultures  will 
usually  reveal  the  presence  of  Bad.  bovisepticum.  The  lesions 
hemorrhagic  in  nature. 

Incase  of  the  "cornstalk  disease"  the  lesions  may  consist 
of  small  hemorrhages  (petechise)  especially  of  the  serous 
membranes  and  heart.     The  cultures  will  be  negative. 

With  anthrax  and  symptomatic  anthrax,  the  specific  bac- 
teria of  these  diseases  will  be  found. 

§  62.  Prevention.  When  this  disease  occurs  it  is  im- 
portant to  remove  the  unaffected  animals  to  other  fields  or  en- 
closures. It  is  well  to  divide  them  into  small  groups  if  pos- 
sible. The  carcasses  of  animals  that  die  should  be  burned  or 
buried  deeply  with  a  good  covering  of  a  disinfectant  such,  for 
example,  as  quick  lime.  Should  death  occur  in  a  stable,  all 
contaminated  litter  should  be  burned  and  the  floors,  mangers 
and  walls  thoroughly  disinfected. 

Experiments  have  been  made  directed  towards  protective 
inoculation,  but  thus  far  the  results  have  not  been  sufficiently 
-satisfactory  to  warrant  the  recommendation  of  the  methods. 

REFERENCES. 

1.  Boi<LiNGER.  Ueber  eine  neue  Wild-und  Rinderseuche.  Munchen. 
1878. 

2.  Fennimore.  wild  and  cattle  disease.  Jour,  of  comp.  iucd .  a^id 
vet.  archiv.     Vol.  XIX  (1898)  p.  625. 

3.  Galtier.  Noveaux  faits  tendant  a  etablir  que  la  pneumo- 
enterite  infectieuse  existe  sur  les  grands  et  les  petits  ruminants  en 
algerie.     Reciieil  de  nied.  veter.,  7  serie..  Vol.  VIII.     1891.     p.  97. 


FOWL    CHOLERA  77 

4.  HuEPPE.  Ueber  die  Wildseuche.  Berlin,  klimsche  IVochenschrift. 
18S6.     p.  753- 

5.  KiTT.  Ueber  eine  Experimentelle,  der  Rinderseuche  (  Bollinger) 
ahnliche  Infektionskrankheit.  Sitzungsberichte  der  Gesellschaft  fiir 
Morphologic  und  Physiologie  in  Miinchen,  I.     1885.     p.  140. 

6.  PioT.     Le  Barbone  du  Buffle.  Bulletin  d.  I' Instil  Egyptian.   1889. 

7.  PoELS.  Septische  Pleuropneumonie  der  Kalber.  Fortschr.  d. 
Med.     1 886.     p.  38S. 

8.  Wilson  and  Brimhall.  Sixty  cases  of  haemorrhagic  septi- 
caemia in  cattle  due  to  Bacillus  bovisepticus.  Report  State  Board  of 
Health  of  Minnesota.     1901.     (Very  full  bibliography. ) 


FOWL  CHOLERA. 


§63.  Characterization.  This  is  an  infectious  disease  of 
fowls  caused  by  bacteria,  and  transmissable  by  cohabitation  and 
inoculation.  It  is  determined  by  a  high  fever,  great  weakness 
and  prostration,  and  usually  terminates  in  the  death  of  the 
affected  bird.  It  is  reported  that  it  attacks  all  varieties  of 
domesticated  poultry  (chickens,  ducks,  geese,  pigeons,  tur- 
keys), and  caged  birds  such  as  parrots  and  canaries.  It  also 
attacks  some  species  of  wild  birds.  It  is  communicable  by 
inoculation  to  rabbits  and  mice.  Guinea  pigs  are  not  verj- 
susceptible. 

§  64.  History.  This  disease  is  mentioned  in  some  of  the 
oldest  works  treating  of  the  disease  of  animals.  Fowl  cholera 
was  studied  by  Chabert  in  1782  who  regarded  it  as  a  form  of 
anthrax.  Since  1825,  it  has  been  frequently  observed  in 
France  where  it  caused  enormous  losses  in  1830,  in  1850  and 
in  i860.  About  1830,  it  became  known  in  Russia,  Bohemia 
and  Austria.  In  1851,  Benjamin  considered  it  to  be  a  con- 
tagious disease  but  remarked  that  people  and  dogs  might  con- 
sume with  impunity  the  meat  of  affected  fowls.  Delafond 
observed  that  it  might  be  transmitted  to  birds  and  rabbits  by 
using  blood,  secretions,  and  portions  of  the  flesh.  It  was  also 
recognized  that  the  excrement  plays  an  important  part  in  the 
dissemination  of  the  virus. 

During  recent  years  it  has  been  observed  in  nearlj^  all  of 
the  countries  of  Europe  as  well  as  in  the  United  States.  It 
has  been  reported  from  many  places  in  the  United  States,  but 


78  FOWL    CHOLERA 

its  presence  seems  to  have  been  determined  by  scientific 
investigation  in  but  a  very  few  of  these.  Salmon  investigated 
it  in  South  Carolina  in  1879-80,  and  Higgins  in  1898  reported 
it  from  Canada.  Salmon  gave  special  attention  to  vaccination 
and  the  effect  of  disinfectants  in  destroying  the  virus. 

Perroncito  was  among  the  first  to  describe  the  specific 
cause  of  the  disease.  This  was  followed  by  the  contributions 
of  Pasteur,  who,  in  1880,  cultivated  the  bacterium  in  chicken 
broth  and  showed  that  its  virulence  might  be  reduced  to  such 
an  extent  that  it  could  safely  be  used  for  vaccination.  This 
is  the  first  case  in  which  a  virulent  organism  was  successfully 
modified  in  a  laboratory  and  made  to  act  as  a  vaccine.  It  was 
the  forerunner  to  the  preparation  of  vaccines  for  a  number  of 
diseases,  more  particularly  for  anthrax,  black  quarter,  and 
rabies. 

§  65.  Geographical  distribution.  Fowl  cholera  seems 
to  be  widely  distributed  in  Europe  and  it  has  been  found  in  a 
few  localities  in  the  United  States  and  in  Canada. 

§  66.  Etiology.  Fowl  cholera  is  caused  by  a  specific 
bacterium  which  is  not  di.stinguishable  morphologically  or  in 
its  cultural  manifestations  from  the  other  members  of  the 
group  of  bacteria  of  which  Bad.  septicaerniae  hemorrhagicac  is 
the  type.  In  this  group  are  the  bacteria  of  rabbit  septicae- 
miae,  swune  plague,  and  Wildseuche.  It  is  a  small  slightly 
elongated  organism  with  rounded  ends.  In  stained  prepara- 
tions from  the  tissues  it  exhibits  a  pronounced  polar  stain. 

§  67.  Symptoms.  The  symptoms  described  for  this 
disease  in  Europe  differ  somewhat  from  those  reported  by 
Salmon.  The  period  of  incubation  is  placed  by  European 
writers  at  from  18  to  48  hours.  In  the  case  of  40  fowls  inocu- 
lated by  Salmon,  it  varied  from  4  to  20  days  the  average 
period  being  8  days.  The  duration  of  the  disease  also  varies. 
Usually  the  sick  birds  stop  eating  or  the  appetite  is  lessened, 
though  occasionally  they  continue  to  eat  almost  to  the  time  of 
death.  The  earliest  indication  of  the  disease,  is  a  yellow- 
coloration  of  the  urates.  In  health,  these  are  a  pure  white 
though  they  are  frequently  tinted  with  yellow  as  the  result  of 
disorders  other  than  cholera. 


SYMPTOMS  79 

Occasionally  the  first  symptom  is  a  diarrhea  in  which  the 
excrement  is  passed  in  large  quantities  and  consists  almost  en- 
tirely of  white  urates  mixed  with  colorless  mucus. 

Very  soon  after  the  first  symptoms  appear  the  bird  sepa- 
rates itself  from  the  flock,  it  no  longer  stands  erect,  the 
feathers  are  roughened,  the  wings  droop,  the  head  is  drawn 
down  towards  the  body  and  the  general  outline  of  the  bird 
becomes  spherical  or  ball  shaped.  At  this  period  there  is 
great  weakness,  the  affected  bird  becomes  drowsy  and  may 
sink  into  a  sleep  which  lasts  during  the  last  day  or  two  of  its 
life,  and  from  which  it  is  almost  impossible  to  arouse  it. 

The  crop  is  nearly  always  distended  with  food  and  appar- 
ently paralyzed.  There  is  in  most  cases  intense  thirst.  If  the 
birds  are  aroused  and  caused  to  walk,  there  is  at  first  an 
abundant  discharge  of  excrement  followed  at  short  intervals 
by  scanty  evacuations. 

With  the  beginning  of  diarrhoea  the  body  temperature 
rises  to  109  or  110°  F.  The  comb  loses  its  bright  hue  and 
becomes  pale  and  bloodless.  In  Europe  the  comb  is  described 
as  dark  blue,  purple,  or  black,  and  some  writers  in  the  United 
vStates  have  referred  to  it  in  the  same  terms.  Salmon  reports 
that  he  has  never  observed  a  dark  comb  in  the  cases  he  has 
seen. 

Diseased  birds  rapidly  lose  in  weight,  they  are  so  weak 
that  a  slight  touch  causes  them  to  fall  over,  and  they  walk 
with  great  difficulty.  The  fowls  become  very  much  emaciated. 
Death  may  occur  without  a  struggle  or  there  may  be  convul- 
sive movements  and  cries. 

This  disease  ma}^  rapidly  run  through  a  flock  destroying 
the  greater  part  of  the  birds  in  a  week,  or  it  may  assume  a 
more  chronic  form,  extend  slowly,  and  remain  upon  the  prem- 
ises for  several  weeks  or  months. 

§  68.  Morbid  anatomy.  The  comb  is  pale  and  blood- 
less. The  superficial  blood  vessels  usually  contain  but  little 
blood,  and  there  are  in  most  cases  soiled  feathers  about  the 
anus,  to  which  the  excrement  may  adhere  in  considerable 
quantity. 

The  liver  is  usually  enormously  enlarged,  softened,  with 


8o  FOWL   CHOLERA 

blood  vessels  engorged.     The  gall  bladder  is  distended  with 
thick  dark  bile. 

The  crop  is  usually  distended  with  food,  though  no 
special  lesions  have  been  noticed  here.  The  stomach  viewed 
externally,  often  presents  a  number  of  circular  discolorations 
about  three  millimeters  in  diameter,  which  on  section  are 
found  to  be  extravasated  blood.  The  small  intestines  are 
congested. 

The  rectum  and  cloaca  usually  present  deep  red  lines 
upon  their  mucous  membrane,  evidently'  the  first  stage  of 
inflammation,  which  results,  in  chronic  cases,  in  thickening 
of  the  walls,  especially  of  the  rectum,  the  desquamation  of  the 
mucous  membrane,  and  the  formation  of  large  ulcerated 
surfaces. 

The  mesentery  is  generally  congested,  often  greatly 
thickened  and  reddened,  and  rendered  opaque  by  inflamma- 
tion. The  ureters  are  distended  with  yellow  urates ;  the 
kidneys  seem  engorged,  and  on  section  accumulations  of  the 
tenacious,  yellow  urates  are  frequently  seen.  The  spleen  is 
generally  normal  in  size  and  appearance,  though  frequently 
enlarged  and  softened. 

The  pericardium  is  sometimes  distended  with  effusions,  in 
which  case  there  is  noticeable  hyperaemia  of  the  surface  of  the 
heart.  The  lungs  are  often,  though  not  generally,  engorged 
with  dark  blood  ;  they  are  seldom,  if  ever,  hepatized. 

The  blood  vessels  are  sometimes  filled  with  a  firm  clot, 
and  contain  but  little  liquid  ;  at  other  times  the  blood  does 
not  coagulate  at  all.  It  seems  to  be  those  cases  in  which  the 
duration  of  the  disease  is  longest,  that  the  blood  loses  its 
power  to  coagulate. 

§  69.  Differential  diagnosis.  Fowl  cholera  is  to  be 
differentiated  (i)  from  a  number  of  dietary  disorders  which 
cause  the  death  of  a  large  number  of  fowls.  These  cases  are 
often  thought  to  be  chicken  cholera  and  so  reported  by  the 
owners.  A  diagnosis  is  to  be  made  in  the  findings  of  a  bac- 
teriological examination.  (2)  Fowl  cholera  is  to  be  differ- 
entiated from  infectious  leukaemia.  There  are  a  number  of 
resemblances  in  the  clinical    history  of  the  two  diseases  but 


PREVENTION  8 1 

there  are  marked  differences  in  both  the  morbid  anatomy  and 
etiolog}-.  For  a  comparison  of  the  lesions  and  specific  bacteria 
of  these  two  diseases  see  infectious  leukaemia. 

§  70.  Prevention.  Pasteur  introduced  a  preventive 
inoculation  or  vaccine  for  this  disease.  Kitt  has  found  that 
the  eggs  of  fowls  unknown  to  this  disease  possessed  a  sub- 
stance somewhat  similar  to  antitoxin.  He  immunized  fowls 
b}'  injecting  them  subcutaneously  with  from  four  to  eight 
cubic  centimeters  of  the  white  of  such  eggs.  While  exceed- 
ingly interesting  this  method  does  not  seem  practicable. 
Good  sanitary  conditions,  isolation  of  the  well  from  the  sick 
fowds  and  thorough  disinfection  seems  to  be  the  most  satis- 
factor}'  procedure.  It  is  important  not  to  introduce  the 
disease  with  newly  purchased  fowls  or  to  expose  healthy  ones 
to  the  disease  either  at  or  in  transportation  to  various  poultry 
exhibits. 

REFERENCES. 

1.  HiGGiNS.  Notes  on  an  epidemic  of  fowl  cholera  and  upon  the 
comparative  production  of  acid  by  allied  bacteria.  Jour,  of  Experi- 
mental Medicine.     Vol.  III.   (1S98J  p.  651. 

2.  Perroncito.  Arch,  fur  wiss.pi-ackt.    Thierheilktinde.  1879.  p.  9. 
3      Pasteur.     De  I'attenuation    du    virus   du    Cholera    der   poules. 

Compies  Rendus  des  Seances  de  V  Academic  des  Sciences.     iSSo.     \'ol. 
XCI.     p.  673. 

4.  Pasteur.  Sur  les  maladies  virulentes,  et  en  particulier  sur  la 
maladie  appelee  vulgairement  cholera  des  poules.  Ibid.  1880.  Vol. 
XC.     p.  239. 

5.  Salmon.  Annual  Reports  of  the  U.  S.  Commissioner  of  Agri. 
culture.     iSSo.     -  82. 

6.  Salmon.  The  diseases  of  poultry.  Washington,  D.  C.  1899. 
p.  232. 


ANTHRAX. 


Synonyms.  Splenic  fever ;  splenic  apoplexy  ;  wool 
sorters'  disease  ;  malignant  pustule  ;  anthracaemia  ;  charbon  ; 
mal-de-rote;  ;  Milzh'and ;  mycosis  intestinalis. 

§  71.  Characterization.  Anthrax  is  an  infectious 
disease  occurring  sporadically  and  is  epizootics  in  herbivora 
and  omnivora  and  communicable  to  nearly  all  warm-blooded 
.animals,  and  to  man.     It  is  characterized  by  the  presence  in 


8l  ANTHRAX 

the  diseased  tissues  or  liquids  oi  Bacterium  anthracis,  by  an 
enlarged  spleen,  blood  extravasations  and  by  local  gangrene. 
It  usually  occurs  in  fhe  acute  form. 

§  72.  History.  Anthrax  is  among  the  oldest  of  the 
known  infectious  diseases  of  animals.  Descriptions  of  epi- 
demics and  epizootics  of  this  disease  are  given  by  Homer, 
Plutarch,  Livy  and  other  writers  before  the  Christian  Era. 
The  Arab  physicians  designated  it  as  "Persian  Fire."  Exten- 
sive outbreaks  are  mentioned  in  the  literature  of  the  fifteenth, 
sixteenth,  seventeenth,  eighteenth  and  nineteenth  centuries. 
Chabert  pointed  out  in  1780  that  the  various  kinds  or  forms 
of  disease,  which  had  previously  been  described  as  independ- 
ent affections,  were  all  one  disease.  As  late  as  1805,  Kausch 
gave  a  good  description  of  anthrax  but  denied  its  contagious- 
ness. Delafond  and  Gerlach  investigated  very  thoroughly 
ovine  anthrax  in  1845  and  its  contagiousness  was  experiment- 
ally shown  by  Gerlach.  In  1850,  Heusinger  published  a  very 
comprehensive  treatise  on  anthrax,  which  dealt  at  length  with 
its  history  and  geographical  distribution. 

Much  new  information  concerning  the  nature  of  anthrax 
was  acquired  during  the  fifth  decade  of  the  last  century.  In 
1855,  Pollander  announced  the  discovery,  which  he  first  made 
in  1849,  of  minute  unbranched  rod  shaped  bodies  in  the  blood 
of  cattle  dead  of  anthrax.  Davaine  observed  similar  bodies  in 
1850.  Then  followed  a  long  series  of  observations  and  some- 
what controversial  discussions  on  the  bacterial  origin  of  the 
disease,  culminating  in  1875  by  Robert  Koch's  careful  descrip- 
tion of  the  morphology  of  its  specific  organism  including  the 
spore  formation.  Cohn,  however,  seems  to  have  been  the 
first  to  have  called  the  organism  a  Bacillus  and  to  have  sus- 
pected the  existence  of  spores.  Toussaint,  in  1880,  and 
Pasteur  in  1881,  published  results  of  investigations  directed 
toward  protective  inoculation.  Since  that  time,  the  literature 
on  the  cause,  morbid  anatomy  and  prevention  of  anthrax  has 
become  very  extensive. 

§  73.  Geographical  distribution.  Anthrax  is  a  widely 
disseminated  disease.  The  continent  of  Europe  has  perhaps 
suffered  most  from  its  ravages.     It  occurs,  also,  in  Northern. 


ETIOI.OGY 


83 


Eastern  and  Central  Africa,  where  in  recent  years  it  has  become 
a  great  plague.  In  Siberia  it  has  caused  fearful  destruction, 
and  in  that  country  it  is  still  known  as  the  "Siberian  Plague." 
It  has  frequently  appeared  in  England.  Russia,  India  and 
Australia  are  also  infected.  In  the  United  States,  it  has  been 
reported  from  at  least  fifteen  states  and  territories.  In  fact 
there  are  very  few,  if  any,  countries  where  this  disease  has  not 
been  found.  In  the  eastern  part  of  this  country  it  exists  to  a 
greater  or  less  extent  in  certain  localities.  A  knowledge  of 
its  .specific  cause  with  the  methods  of  properly  disposing  of 
dead  animals,  isolation  and  disinfection  as  well  as  the  pre- 
ventive inoculations  now  in  vogue,  have  made  it  possible  to 
prevent  widespread  epizootics.  In  America  it  is  looked  upon 
as  a  comparatively  rare  disease,  excepting  in  certain  infected 
districts. 

§  74.  Etiology.  An- 
thrax is  due  to  the  effect  of 
the  presence  of  a  specific 
micro-organism  known  as 
Bacterium  {Bacilhis^  an- 
thracis.  This  organism  is 
found  in  the  diseased  tissues 
and  organs  of  affected  ani- 
mals. On  account  of  its 
spores,  it  is  very  resistant 
to  the  normal  destructive 
agencies  in  nature.  Con- 
sequently when  it  is  once 
introduced  into  a  locality  it  p^^.  10.    Anthrax  bacteria  from  an 

tends  to  remain  there  for  impression  preparation  from  a  colo^iy. 
many  years,  possibly  causing  from  time  to  time  a  few  cases  of 
anthrax  or  serious  epizootics  or  epidemics.  The  spores  are 
also  frequently  carried  in  the  wool,  hair,  hide,  hoofs  and  horns 
taken  from  animals  sick  or  dead  of  anthrax.  Thus  the  affec- 
tion has  been  introduced  into  far  distant  localities. 

Bacterium  anthracis  is  a  rod-shaped  organism  varying  in 
length  from  i  to  4//,  but  having  a  quite  uniform  breadth  of 
about  one  micron.     In  a  suitable  medium  it  grows  out  in  long 


84  ANTHRAX 

flexible  filaments,  which  combine  to  form  thread-like  bundles. 
When  examined,  the  ends  of  the  rods  seem  to  be  square  cut. 
In  preparations  from  animal  tissues  there  appear  sometimes  to 
be  slight  concavities  in  the  ends  of  the  segments  when  two  of 
them  are  united.  In  old  cultures  spores  are  formed.  These 
are  oval,  highly  refractive  bodies  held  within  the  cellular 
envelope  of  the  filaments,  but  later  they  are  set  free  by  the 
dissolution  of  this  membrane.  It  stains  readily  with  the  ani^ 
line  dyes  and  also  by  Gram's  method. 

B 


Fig.  II.     Bacterium  anthracis.     A.  without  spores.     B.  with  spores. 

The  bacterium  of  anthrax  itself  is  not  an  especially  hardy 
organism.  On  the  contrary  it  is  easily  destroyed  by  weak 
disinfectants  and  it  has  a  low  thermal  death  point.  Its  spores, 
however,  are  among  the  most  hardy  of  bacterial  life  to  resist 
chemical  and  thermal  agents.  They  resist  drying  for  months 
or  years  and  often  boiling  for  a  half  hour  or  longer  does  not 
destroy  them.  On  this  account  it  is  very  difficult  to  eliminate 
the  virus  from  infected  pasture  lands,  especially  if  they  are 
wet  or  marshy. 

As  the  spores  may  remain  in  the  soil  in  a  dormant  condi- 
tion for  many  years  it  sometimes  happens  that  the  disease  does 
not  appear  until  long  after  the  introduction  of  the  virus. 
Anthrax  has  been  known  to  break  out  among  cattle  grazing 
on  a  field  in  which  the  carcasses  or  hides  from  affected 
animals  were  buried  many  years  before.  Through  some 
means  the  spores  were  able  to  get  to  the  surface  and  contami- 
nate the  grass.     The  virus  may  be  introduced  with  blood  or 


CHANNELS    OF    INFECTION 


85 


Fig.  12.     Anthrax   bacteria    in   a  cover-glass  preparation  of  blood 
showing  chains  and  capsules. 


bone  fertilizers,  hides,  hair  or  wool  from  infected  countries. 
When  the  extent  of  this  traffic  is  realized,  it  is  easy  to  under- 
stand how  anthrax  has  been  brought  to  this  countrj^  and  why 
it  occasionally  appears  heie  and  there  over  a  large  part  of  the 
continent.  Many  outbreaks,  as  well  as  isolated  cases,  illus- 
trating this  common  method  of  dissemination  are  on  record. 

J^  75.  Animals  attacked.  Nearly  all  animals  suffer 
from  anthrax.  The  herbivora  and  rodents  are  most  suscepti- 
ble. It  is  interesting  to  note  that  the  Algerian  race  of  sheep 
are  immune.  A  satisfactory  explanation  for  this  striking 
exception  has  not  been  recorded.  It  has  been  stated  that  a 
single  bacterium  introduced  into  the  subcutaneous  connective 
tissue  of  a  guinea-pig  or  mouse  is  sufficient  to  kill.  Cats, 
tame  and  wild  rabbits,  and  hares  are  the  next  most  susceptible 
species.  It  is  stated  that  dogs,  pigs,  and  foxes  are  very 
slightly  susceptible.  Rats,  fowls  and  pigeons  are  reported  to 
be  immune.      Fish  and  amphibia  are  rarely  attacked. 

§  76.  Channels  of  infection.  Three  common  modes  of 
infection  are  recognized  for  anthrax,  namely  :  through  the 
digestive  tract,  by  the  skin  and  by  the  lungs.  In  cattle  the 
infection  seems  to  be  largely  through  the  alimentary  canal  ; 
in  horses  and   sheep  by  the  skin   or  digestive  tract  ;  in  men 


86  ANTHRAX 

through  wounds  of  the  skin  and  the  respiratory  tract.     There 
are,  however,  many  exceptions  to  these  usual  methods. 

(i.)     Infection  through  the  alimentary  canal.     This  is  the 
more  common   mode    of  infection    in    cattle.     The    resulting 
disease  has  been  designated  by  various  names  among  which 
are    "intestinal  anthrax,"    "fodder  anthrax,"    "spontaneous 
anthrax,"  "internal  anthrax,"  "anthrax  fever,"  and  anthrax 
without  external  manifestations.     In  these  cases  the  infecting 
organisms,   either  the  spores  or  the  bacteria  themselves,  are 
taken  into  the  body  with  food  or  drinking  water.      It  is  stated 
that  the  infection  takes  place  in  most  cases  in  the  small  in- 
testine, the  mucosa  of  which,  it  is  stated,  need  not  necessarily 
be    injured.       It    is    highly    probably    that    the    gastric  juice 
destroys  most  of  the  bacteria  while  the  free  spores  are  not  injur- 
iously affected  by  it.     In  infected  districts  the  spores  exist  at 
or  upon  the  surface  of  the  soil  and  possibly  on  the   blades  of 
grass  from  which  they  are  easily  taken  up  by  grazing  animals. 
In  cases  thus  infected  the  specific  organism  has  been  intro- 
duced  at   some  previous  time  either   (a)    by   the  burying   of 
diseased  animals  in  these   fields,  (b)  by   the   use   of  infected 
tannery  or  slaughter  house  refuse  as  fertilizers,  (c)  by  flood- 
ing from  infected  streams,  or  (d)  by  the   bringing  of   the  or- 
ganism in  the  droppings  of  birds  or  other  small  animals  which 
have  fed  upon  anthrax  carcasses.     It  is  reported  that  the  spores 
will  find  their  way  to  the  surface  even  when  the  dead  animals 
have  been  buried   at  a   considerable   depth.     There  has  been 
some  controversy  in  the  writings  of  Pasteur,  Koch    and  Bol- 
linger concerning  the  method  by  which  the  spores  reach  the 
surface.      Pasteur  supposed   that  they  were  brought  by  earth 
worms  from  the  buried  carcasses.     Koch  believed  this  impos- 
sible because  of  the   low   temperature  of  the  ground  at  the 
depth  at  which  the  animals  are  buried.      Bollinger  has  shown 
experimentally  the  possibility  of  Pasteur's  views.      Karliniski 
and  others  have  found  that  the  spores  of  anthrax  may  be  dis- 
seminated by  slugs,   insects  and  larvae   which   are  found  on 
untanned  infected  skins. 

(2.)     Infection  through  the  skin.      In  animals,  this  mode 
of  infection  occurs  less   frequently   than   in  man.     Anthrax 


ANTHRAX  87 

produced  in  this  way  is  usually  characterized  by  local  mani- 
festations known  as  "carbuncle  disease,"  or  "malignant 
pustule."  In  this  mode  of  infection  the  bacteria  penetrate, 
through  wounds  in  the  skin  and  exposed  mucous  membranes, 
into  the  living  tissues  by  means  of  infected  utensils,  the  use  of 
infected  instruments,  and  the  bites  of  insects,  especially  the 
house  fly  {Afiisca  do7nestica. )  Dairy mple  has  called  attention 
to  the  spread  of  this  disease  among  animals  in  the  lower 
Mississippi  Valley  by  means  of  the  horse  fly  (  Tabanidae. )  In 
man  many  cases  of  the  disease  occur  from  the  injuries  or  cuts 
made  at  the  post-mortem  of  anthrax  animals  or  by  the  infec- 
tion of  skin  wounds  while  handling  infected  hides  or  wool. 
Malignant  pustule  is  reported  to  be  quite  common  among  the 
employes  of  certain  tanneries  and  upholstering  establishments 
where  hides  and  hair  imported  from  infected  districts  or  coun- 
tries are  used. 

(3.)  Infection  through  the  respiratory  tract.  Faser,  Buch- 
ner,  I^emke,  and  other  writers  have  shown  experimentally 
that  the  disease  can  be  produced  by  the  inhalation  of  spores. 
In  man  this  form  of  infection  is  quite  common  among  the  wool 
sorters.  In  Great  Britain  where  much  foreign  wool  is  handled 
it  has  been  reported  as  causing  as  many  as  500  deaths 
annually. 

^  77.  Symptoms.  In  anthrax,  the  symptoms  var}-  not 
only  in  different  species  of  animals  but  also  in  different  indi- 
viduals according  to  the  location  of  the  disease.  Again,  there 
is  often  considerable  variation  when  the  lesions  are  apparently 
the  same.  The  most  characteristic  features  of  the  disease  are 
(i)  the  suddenness  of  the  attack,  (2)  the  grave  general  distur- 
bances, (3)  high  elevation  of  temperature,  (4)  a  tendency  to 
ecchymoses  of  the  mucous  membranes  and  (5)  local  manifes- 
tations, such  as  carbuncles  and  oedema  of  the  skin,  digestive 
disturbances,  brain  complications  or  difficult  respiration.  It 
sometimes  happens  that  symptoms  of  metastatic  infection 
are  detected. 

Anthrax  has  been  classified  according  to  its  course  as  per- 
acute,  acute  and  subacute.      It  has  also  been  divided  accord- 


88  SYMPTOMS 

ing  to  the  site  of  its  manifestations  as  anthrax  with  visible 
localization,  and  anthrax  without  visible  localization. 

A7ithrax  without  visible  localization.  This  form  is  gener- 
ally due  to  ordinary  infection  presumably  by  spores.  It  in- 
cludes the  peracute,  acute,  and  subacute. 

(i)  The  peracute  or  apoplectic  anthrax  gives  rise  to 
symptoms  of  cerebral  apoplexj'.  The  animal  becomes  sud- 
denly ill,  staggers  about  for  a  brief  period  and  falls.  There  is 
often  a  bloody  discharge  from  the  mouth,  nostrils  and  anus. 
Death  usually  ensues  in  from  a  few  minutes  to  an  hour. 
Usually  there  are  convulsions.  Sheep  and  cattle  suffer  most 
frequently  from  this  form  of  the  disease.  They  are  often 
found  dead.  This  is  especially  true  in  the  beginning  of  an 
epizootic. 

(2)  In  the  acute  form  the  disease  runs  a  somewhat 
slower  course,  lasting  usually  not  to  exceed  twenty- four  hours. 
The  temperature  rises  rapidly  to  from  105  to  108°  F.  With 
this  there  are  signs  either  of  congestion  of  the  brain  or  of  the 
lungs.  If  the  brain  is  affected  the  animal  becomes  restless, 
excited,  stamps  the  ground,  rears  in  the  air,  bellows,  runs  to 
and  fro  and  finally  goes  into  convulsions  followed  by  stupor 
and  death.  If  the  lungs  are  congested  there  is  difficulty 
in  breathing,  more  or  less  wheezing,  panting,  groaning,  palpi- 
tation of  the  heart,  small  and  frequent  pulse,  cyanosis  of  the 
mucosa  of  the  head,  bloody  discharges,  haematuria,  stagger- 
ing and  finally  convulsions  and  death  from  suffocation. 
Occasionally  there  is  a  partial  remission  of  the  symptom,  fol- 
lowed by  relapse.  It  has  been  observed  that  occasionally 
there  are  premonitory  symptoms  preceding  the  acute  attack 
consisting  of  slight  digestive  disturbances  and  diminished 
vivacit3^ 

(3)  The  subacute  form  is  known  as  anthrax  fever  or  in- 
termittent anthrax.  The  symptoms  are  the  same  as  in  the 
other  forms,  excepting  they  are  more  sharply  defined  and  the 
course  is  longer.  The  disease  lasts  from  one  to  seven  or  eight 
days,  the  average  being  about  forty-eight  hours.  The  high 
temperature,  the  congestion  of  the  lungs  or  brain  complicated 
with  intestinal  disturbances,  especially  colic,  are  usually  well 


ANTHRAX  89- 

marked.  In  epizootics  where  the  peracute  or  acute  form 
ushers  in  the  disease,  the  later  cases  usually  are  of  the  sub- 
acute variety.  It  often  happens  that  the  last  animals  attacked, 
exhibit  the  subacute  or  more  chronic  form. 

Antht'ax  with  visible  localization.  These  forms  usually  re- 
sult from  infection  of  the  skin  and  mucous  membranes.  The 
lesions  are  spoken  of  as  carbuncles  and  often  there  is  marked 
local  oedema  of  the  skin.  This  form  is  common  in  man, 
horses  and  sometimes  in  cattle.  It  is  reported  to  occur  in  other 
species.  The  carbuncles  are  circumscribed,  cutaneous  swellings 
which  are  at  first  hard,  hot  and  painful.  Later  they  become 
cold  and  painless  with  a  tendency  to  become  gangrenous.  The 
oedematous  tissue  becomes  dough}^,  cold  and  painless  ;  fre- 
quently fluctuating  swellings  of  the  skin  occur.  The  duration 
of  this  form  of  the  disease  varies  from  four  to  fifteen  days. 
Ordinarily  it  is  not  so  fatal  as  internal  anthrax. 

When  the  infection  is  on  the  mucous  membrane  the  animal 
suffers  from  fever,  dyspnoea,  difficulty  in  swallowing,  and 
cyanosis,  together  with  the  immediate  local  effects.  Death  oc- 
curs much  sooner  than  when  the  disease  is  located  on  the  skin. 
It  is  stated  that  dogs  and  swine  suffer  from  this  form  more 
than  from  the  more  acute  types. 

In  horses,  anthrax  usually  runs  an  acute  or  subacute 
form.  The  first  symptom  is  rise  of  temperature  with  a  rapid, 
feeble  pulse.  Occasionalh'  there  are  chills  and  muscular 
spasms.  The  mucosa  of  the  head  becomes  cyanotic  and  lacry- 
mation  is  often  present.  The  animal  has  a  dull,  stupid  look, 
appears  to  be  stunned  and  walks  with  a  staggering  gait.  In 
some  cases  there  are  symptoms  of  cerebral  congestion  such  as 
restlessness  or  convulsions.  Colic  is  a  very  characteristic 
sj-mptom  in  the  horse,  otherwise  the  symptoms  are  the  same 
as  in  cattle.  Infection  of  the  skin  usually  occurs  on  the 
hypogastrium,  lower  part  of  the  breast,  inner  surface  of  the 
fore  and  hind  quarters.  Swelling  of  the  hind  quarters  often 
causes  lameness.  Carbuncles  of  the  mucous  membrane  of  the 
tongue  is  said  to  occur  rarely  in  these  species. 

In  sheep  and  goats  the  disease  is  usually  of  the  acute  or 
apoplectic  form.     The  animals  appear  as  if  suddenly  stricken 


90 


MORBID    ANATOMY 


with  apoplexy.  If  death  does  not  occur  within  a  very  short 
time,  symptoms  heretofore  described  for  this  form  of  the 
disease  may  be  recognized.  Subacute  anthrax  is  said  to  be 
very  rare  in  sheep. 

In  swine,  anthrax  is  ordinarily  characterized  by  local 
lesions  on  the  mucous  membrane  of  the  larynx  or  pharynx. 
The  animals  have  a  rise  of  temperature  and  the  intermaxillary 
space  is  generally  swollen.  The  swelling  may  spread  along 
the  trachea  giving  rise  to  difficulty  in  swallowing,  hoarseness, 
cyanosis  of  the  mucosa  of  the  mouth,  dyspnoea  and  rapid 
breathing.  The  animal  shows  signs  of  paralysis.  Death 
occurs  from  suffocation.  Frequently  the  tongue  becomes  the 
seat  of  the  disease.  Carbuncles  occuring  on  the  skin ,  especially 
of  the  back,  have  been  described  in  this  species. 

In  dogs  and  cats,  the  disease  u.sually  runs  a  very  rapid 
course.  The  fact  that  they  are  usually  infected  by  eating  the 
meat  of  animals  dead  of  anthrax  causes  them  to  suffer  largely 
from  the  intestinal  form.  It  has  been  stated  that  probably 
much  of  the  so  called  anthrax  in  dogs  was  simply  cases  of 
ptomaine  poisoning. 

It  is  reported  that  in  birds  anthrax  usually  runs  a  very 
rapid  and  usually  fatal  course.  Toward  the  end  they  stagger, 
tremble,  or  go  into  convulsions,  and  die  with  bloody  discharges 
from  the  mouth,  nostrils,  and  anus.  From  the  first  the  birds 
are  depressed  and  weak,  their  feathers  ruffled  and  wangs 
drooping.  There  is  evidence  of  dyspnoea  and  bloody  diar- 
rhoea. Occasionally  carbuncles  appear  on  the  comb,  wattles, 
conjunctiva,  tongue  and  extremities. 

It  has  been  stated  that  the  milk  from  cows  suffering  with 
anthrax  contains  Bad.  anthracis.  The  writer  found  in  the 
examinations  made  in  one  epizootic  that  the  anthrax  bacteria 
were  present  in  considerable  numbers  in  the  milk  just  before 
or  immediately  after  death,  but  they  were  not  found  in  the 
milk  of  animals  in  the  earlier  stages  of  the  disease. 

§  78.  Morbid  anatomy.  The  nature  and  extent  of  the 
tis.sue  changes  depend  upon  the  course  of  the  disease.  When 
experimentally  produced  it  is  ordinarily  a  septicaemia.  This 
form  often  occurs  in  the  domesticated  animals  that  contract  the 


ANTHRAX  gr 

disease  naturally.  The  more  common  anatomical  changes, 
except  in  the  most  acute  cases  and  in  the  strictly  localized 
lesions  or  carbuncles  are:  (i)  Hemorrhages  varying  in 
amount  from  petechiae  to  blood  extravasations,  with  more  or 
less  serous,  gelatinous  and  hemorrhagic  infiltration  of  the 
submucous,  subserous  and  subcutaneous  tissue  ;  (2)  Enlarge- 
ment of  the  spleen  with  parenchymatous  inflammation  of  the 
liver  and  kidneys  ;  (3)  A  dark  tar-like  condition  of  the 
blood  ;  and  (4)  The  presence  in  the  tissues  and  blood  of 
Bacterium  anthracis.  In  the  ver}-  acute  cases  these  changes 
are  often  slight,  while  in  the  more  chronic  forms  they  are 
strongh'  marked.  It  is  important  to  note  that  occasionally 
the  usual  changes  indicated  by  the  symptoms  and  the  duration 
of  the  disease  are  not  found  on  post-mortem  examination.  In 
one  epizootic,  the  writer  has  seen  an  animal  dead  from  sub- 
acute anthrax  in  which  the  blood  and  tissues  were  teeming 
with  anthrax  bacteria,  yet  the  organs  appeared  to  be  perfectly 
normal.  Other  animals  in  the  same  outbreak  exhibited  the 
more  usual  anatomical  changes. 

The  blood  is  usually  very  dark  and  tar-like  in  appearance. 
The  cutaneous  capillaries  are  di.stended  and  frequently  there  are 
hemorrhages  beneath  the  epidermis.  The  subcutis  is  sprinkled 
with  ecchymoses.  Frequently  there  are  gelatinous  effusions 
of  a  rather  firm  consistance  and  of  varying  size.  The  color 
also  differs,  ranging  between  a  deep  yellow  and  a  3'ellowish 
brown.  Often  these  oedematous  areas  are  sprinkled  with 
hemorrhagic  foci.     A  simple  serous  oedema  may  occur. 

The  lymphatic  glands  may  be  hemorrhagic  or  oedematous 
or  both.  Frequently  an  oedematous  condition  of  the  connective 
tissues  of  the  neck  or  about  the  trachea  is  very  marked. 

The  muscles  vary  in  color  but  usually  they  are  darker 
than  normal,  and  like  the  skin,  they  often  become  sprinkled 
with  ecchymoses.  The  heart  muscle  suffers  from  parenchy- 
matous changes  (myocarditis). 

In  the  larger  cavities  of  the  body,  a  sanguinolent  fluid  is 
found  in  moderate  quantities.  Blood  extravasations  of  differ- 
ent sizes  are  seen  under  the  serous  membranes,  particularly  on 
the   mesentery  and  mediastinum.     The  subserous  connective 


-92  MORBID    ANATOMY 

tissue,  especially  on  tl;e  mesentery,  anterior  cavity  of  the 
mediastinum,  and  in  the  neighborhood  of  the  kidneys,  is  often 
infiltrated  with  a  gelatinous  substance.  On  this  account  the 
neighboring  lymph  glands  are  considerably  swollen,  filled 
with  serum  and  sprinkled  with  hemorrhages.  The  internal 
organs  contain  a  large  quantity  of  blood.  All  the  larger  veins 
and  the  heart  are  filled  with  blood,  while  the  surrounding 
tissues  show  sanious  imbibition. 

The  spleen  is  considerably  enlarged  (two  to  five  times  its 
normal  size),  either  uniformly  or  by  prominent  tumors.  The 
pulp  is  soft,  more  or  less  fluid,  and  stained  dark  red.  The 
capsule  of  the  spleen  is  always  very  tense  and  is  frequently 
-extravasated  with  blood.  Sometimes  small  raised  vesicles  are 
to  be  seen  on  its  surface. 

The  liver  and  kidneys  are  highly  congested  and  somewhat 
enlarged.  The  parenchyma  contain  areas  of  blood  infiltration 
and  the  cells  themselves  manifest  various  kinds  of  degenera- 
tion. The  portal  lymph  glands  often  appear  enlarged,  and  the 
retroperitoneal  tissue  may  be  infiltrated  with  a  serous,  gela- 
tinous fluid.  The  subperitoneal  tissue  of  the  intestines  and 
of  the  abdominal  walls  may  be  similarly  affected. 

The  nature  of  the  lesions  of  the  intestinal  canal  varies 
according  as  the  disease  is  intestinal  anthrax,  or  anthrax 
caused  by  inoculation.  In  cases  of  inoculation-anthrax,  the 
intestine  is  frequently  normal.  In  other  cases  there  may  be 
submucous  and  subserous  hemorrhages,  or  swelling  of  the 
mesenteric  glands.  The  principal  changes  in  intestinal  anthrax 
are  always  found  in  the  small  intestine,  chiefly  in  the  duo- 
denum, more  rarely  in  the  colon.  In  the  milder  cases  of  intes- 
tinal anthrax  the  mucous  membrane  is  affected,  sometimes  by 
circumscribed,  or  diffuse  swellings.  The  specific  bacteria  are 
often  found  in  very  large  numbers  on  the  surface  of  the 
mucous  membrane.  Necroses  and  ulcers  appear  in  those  parts 
where  the  bacteria  are  most  thickly  congregated.  In  very  severe 
cases,  the  abomasum  or  the  first  stomachs  .ii<fey  be  affected  with 
gelatinous  and  sanious  infiltrations  of  the  mucous  membrane. 
The  mucosa  of  the  abomasum,  and  especially  of  the  duodenum, 
is,  in  consequence  of  excessive  hyperaemia,  dark  red  or  almost 


ANTHRAX 


93 


black,  and  is  covered  with  erosions  and  ulcers  or  necroses 
which  may  extend  down  to  the  submucosa.  The  contents  of 
the  intestine  are  bloody,  and  the  submucosa  is  infiltrated  with 
a  serous,  gelatinous,  or  hemorrhagic  exudate,  so  that  the 
mucous  membrane  often  projects,  in  the  form  of  large  tumors, 
into  the  lumen  of  the  intestine.  On  the  site  of  Peyer's 
patches  and  the  solitary  follicles  we  may  find  flat  or  prominent 
nodules,  the  surface  of  which  are  covered  with  diphtheritic 
crusts. 

The  lungs  are  greatly  congested,  oedematous  and  show 
areas  of  ecchj^moses.  The  entire  respiratory  mucous  mem- 
brane is  considerably  reddened  and  affected  by  ecchymoses. 
The  mucous  membrane  of  the  pharynx  and  opening  of  the 
larynx  is  often  so  oedematous  that  stenosis  of  the  larynx  takes 
place.  The  contents  of  the  trachea  and  the  bronchi  consist 
mostly  of  bloody  froth  or  mucus. 

The  brain  is  often  studded  with  ecchymoses.  The  surface  of 
its  membranes  often  exhibits  hemorrhages  with  an  accumulation 
of  sanious  serum  in  the  ventricles.  Extravasations  of  blood 
sometimes  occur  on  the  anterior  chamber  of  the  eye  and  under 
the  retina.  All  the  other  organs  show  hemorrhages,  and  the 
urine  frequently  contains  blood. 

The  blood  is  very  dark,  has  a  tarry  or  varnish  like  lustre, 
and  shows  little  tendency  to  coagulate.  It  does  not  assume  its 
normal  red  color  when  exposed  to  the  air.  The  red  blood 
corpuscles  are  more  of  less  changed.  The  number  of  leuco- 
cytes is  considerably  increased. 

The  bodies  of  animals  which  have  died  from  anthrax  are 
often  well  nourished.  Rigor  mortis  is  absent  and  they  decom- 
pose quickly.  Very  frequently  blood  flows  from  the  natural 
openings  of  the  body,  and  the  rectum   is  sometimes  prolapsed. 

All  the  foregoing  lesions  may  be  absent  in  very  acute 
apoplectic  cases.  The  specific  organism  is,  however,  always 
present  in  the  cadaver. 

§  79.  Differential  diagnosis.  It  is  important  not  to 
confuse  anthrax  with  a  number  of  non-specific  disorders  and 
accidental  causes  of  death.  The  suddenness  of  the  attack,  and 
in  very  virulent  cases,  the  short  duration  of  the  disease  may  tend 


94  DIFFERENTIAL   DIAGNOSIS 

to  the  mistaking  of  it  for  poisoning,  cerebral  apoplexy,  pul- 
monary congestion,  heat  apoplexy,  death  from  lightning,  or 
acute  gastro-intestinal  inflammation.  The  affection  known  as 
corn  stalk  disease  is  not  infrequently  taken  for  anthrax  and 
vice  versa.  In  all  of  these  cases  the  doubt  following  the  post- 
mortem can  be  easily  settled  by  a  bacteriological  examination 
which,  with  genuine  anthrax,  will  reveal  the  presence  of 
Bacterhun  anthracis. 

There  are,  however,  certain  specific  diseases  from  which 
anthrax  must  be  differentiated.  The  more  important  of  these 
are  symtomatic  anthrax  (black  leg),  malignant  oedema,  and 
septicaemia  hemorrhagica.  Rabies  is  not  infrequently  taken 
for  anthrax.  If  the  diagnosis  cannot  be  determined  by  the 
anatomical  changes  (which  can  be  relied  upon  only  in  some- 
what typical  cases)  the  positive  diagnosis  can  be  made  only  with 
the  finding  of  the  anthrax  bacteria.  In  animals  just  dead,  where 
decomposition  has  not  begun,  these  organisms  can  usually  be 
found  in  properly  stained  cover-glass  preparations  made  di- 
rectly from  the  blood  or  tissues.  After  decomposition  begins  to 
take  place,  a  putrefactive  organism,  that  is  not  easily  distin- 
guished from  that  of  anthrax,  often  appears  in  the  tissues.  It 
is,  therefore,  necessary  in  such  cases  to  resort  to  culture  meth- 
ods before  a  positive  statement  can  be  made.  As  the  bacilli  of 
malignant  oedema  and  symptomatic  anthrax  are  anaerobes, 
they  will  not  develop  in  aerobic  cultures  such  as  on  slant 
agar  or  in  bouillon.  The  bacterium  of  septicaemia  hemor- 
rhagica being  a  small  oval  organism  is  easily  told  from  that  of 
anthrax.  Bacillus  subtilis  has  occasionally  been  taken  for  the 
anthrax  bacterium  ;  but  it  is  readily  separated  morphologially 
and  in  cultures,  especially  in  bouillon,  where  subtilis  forms  a 
firm,  wrinkled  membrane  over  the  surface  of  the  liquid  which 
remains  clear  while  the  anthrax  organisms  grow  in  fiocculi 
within  the  medium.  It  is  important  to  recognize  the  possi- 
bility of  error,  if  the  conditions  restrict  the  examination  to  the 
study  of  the  microscopic  preparations. 

iv  80.  Protective  inoculation.  Toussaint  was  the  first  to 
make  use  of  protective  inoculations  in  anthrax.  He  heated 
defibrinated  anthrax  blood  to  a  temperature  of  50  to  55°  C.  for 


ANTHRAX  g^ 

from  15  to  20  minutes  then  injected  it  as  a  protective  agent. 
Pasteur,  however,  was  the  first  to  prove  that  immunity  could 
be  obtained  by  the  use  of  cultures  of  attenuated  bacteria. 
Several  methods  of  attenuating  the  specific  organisms  have 
been  proposed  by  Pasteur,  Toussaint,  Chaveau,  Chamberland, 
Arloing  and  others. 

Pasteur's  method  consists  in  inoculating  the  animal  with 
a  small  quantity  of  a  culture  which  has  been  grown  at  a  high 
temperature— 42  to  43°  C— for  several  days.  This  deprives 
the  bacteria  of  their  virulence.  To  strengthen  the  resistance, 
the  animals  are  again  inoculated  with  a  stronger  virus.  After 
the  two  inoculations,  they  are  said  to  be  protected  against  the 
most  virulent  anthrax  ;  but  the  immunity  is  of  short  duration. 
Chamberland  reported  in  1894  that  a  total  of  1,988,677  animals 
had  been  treated  by  this  method  in  France,  and  that  the  loss 
from  anthrax  had  diminished  from  10  per  cent,  in  sheep  and  5 
per  cent,  in  cattle  to  less  than  i  per  cent.  Cope,  in  his  report 
to  the  English  Board  of  Agriculture,  regards  the  conclusions 
of  Chamberland  as  somewhat  fallacious,  because  in  order  to 
prove  that  the  animals  inoculated  received  immunity,  it  should 
be  shown  that  they  were  subsequently  exposed  to  the  risks  of 
natural  infection.  The  excellent  work  which  has  been  done 
by  Xeal  and  Chester,  at  the  Delaware  College  Experiment 
Station,  has  shown  the  possible  efficiency  of  this  method.  Of 
the  331  cows  which  they  vaccinated  against  anthrax,  two  died 
of  the  disease,  giving  a  death  rate  of  less  than  i  per  cent,  and 
this  in  a  territory  so  saturated  with  the  virus  that  it  was  prac- 
tically impossible  to  keep  cattle  at  all  before  its  use. 

A  more  critical  study  of  the  reports  on  the  use  of  this 
vaccine  shows  that  while  success  can  not  be  denied,  failures 
must  be  admitted.  It  is  reported  both  in  England  and 
Germany  that  the  Pasteur  vaccine  has  not  been  a  marked  suc- 
cess. In  England,  Klein,  w^ho  tested  the  vaccine  used  in  that 
country,  found  that  if  the  animals  did  not  die  from  the  effect 
of  the  vaccine,  they  did  when  exposed  to  the  disease.  The 
German  veterinarians  and  agriculturalists  agree  that  the  first 
vaccine  is  mild  and  harmless,  but  that  the  second  vaccine, 
even  in  the  hands  of  experts,  is  dangerous  and  often  fatal. 


•96  PROTECTIVE    INOCULATION 

The  fact  is  reported  to  have  been  demonstrated  by  experiment 
that  the  virulence  of  the  attenuated  virus  can  be  easil}-  res- 
tored. Again,  it  has  been  shown  by  the  investigations  of 
Chester  and  Neal,  of  the  Delaware  College  Agricultural  Ex- 
periment Station,  that  a  vaccine  which  succeeded  at  one  time 
subsequently  proved  fatal.  The  vital  objection  to  this  method 
is,  that  it  requires  the  use  of  the  living  bacteria  which  later 
may  become  virulent  and  consequently  cause  a  subsequent 
outbreak.  The  scattering  of  pathogenic  organisms,  even  in 
an  attenuated  condition,  should  be  avoided,  if  possible.  It 
must  be  admitted,  however,  that  Pasteur's  method  has  done 
much  good  and  helped  to  rob  anthrax  of  much  of  its  former 
terror,  especiall}-  for  the  farmers  of  Europe.  In  America  the 
spread  of  anthrax  has  been  checked  in  many  districts  by  its 
use.  Dalrj'mple  has  recently  pointed  out  its  success  in  the 
lower  Mississippi  valley.  Notwithstanding,  it  is  highly  pro- 
bable that  the  spreading  of  a  knowledge  of  the  specific  cause 
of  this  disease  with  that  of  proper  disposition  of  dead  animals 
has  also  exerted  much  influence  for  good  in  checking  its  rav- 
ages. 

In  Germany  and  England  the  stamping-out  system  is  con- 
sidered superior  to  vaccination.  According  to  Crookshank,  in 
England  it  is  regarded  as  the  only  reliable  means  of  suppress- 
ing the  disease.  To  this  end  rigid  laws  have  been  enacted. 
In  this  countr}-  as  rigid  measures  as  possible  for  its  eradication 
seem  infinitely  better  than  the  general  adoption  of  methods  for 
establishing  a  tolerance  for  its  existence. 

§  81.  Law's  modification  of  Toussaint's  method. 
Eaw  has  followed  with  marked  success  a  modification  of  Tous- 
saint's  method.  This  consists  in  heating  the  blood  taken  from 
an  animal  just  dead  from  anthrax  or  killed  in  the  last  stages  of 
the  disease,  to  the  boiling  point  of  water,  grinding  it  in  a  little 
sterile  water  or  bouillon  and  injecting  the  resulting  liquid. 
The  writer  has  employed  this  method  in  two  outbreaks  where 
immediate  action  was  imperative.  In  one  of  the  epizootics 
where  it  was  tried,  the  deaths  had  reached  three  a  day  and  the 
astonishing  result  followed  that  not  an  animal  died  after  the 
injection.     In  the  second  outbreak  the  blood  injection  produced 


ANTHRAX  97 

HO  apparent  diminution  in  the  extent  of  the  disease.  It  was 
followed  with  Pasteur's  vaccine  with  very  satisfactory  results. 
It  has  not  been  demonstrated,  however,  that  the  sudden  check 
in  the  spread  of  the  disease  was  not  a  coincidence  rather  than 
the  effect  of  the  blood.  A  single  experiment  in  cattle  to  test 
the  efficiency  of  the  heated  blood  in  protecting  against  anthrax 
inoculation  gave  negative  results.  The  same  held  true  for  ex- 
periments with  guinea  pigs.  Loeffler  has  already  pointed  out 
the  fact  that  small  experimental  animals  are  not  readily 
immunized  to  anthrax. 

The  disposition  of  dead  animals  in  an  outbreak  of  anthrax  is 
a  matter  of  much  importance.  In  all  cases  they  should  be  burned 
if  possible,  if  not,  they  should  be  buried  deeph' and  thoroughly 
covered  with  quick  lime  before  the  dirt  is  replaced.  The  ground 
over  the  place  where  they  are  buried  should  be  fenced  in  to 
prevent  other  animals  from  grazing  over  it  and  the  surface 
should  be  burned  annually  for  some  years  to  destroy  spores 
should  they  be  brought  to  the  surface.  In  all  cases  the  well 
animals  should  be  removed  from  the  barns  or  j-ards  containing 
the  sick  ones  and  from  pasture  lands  on  which  the  sick  became 
infected.  The  temperature  of  the  supposedly  healthy  and  un- 
infected animals  should  be  taken  morning  and  evening  for  from 
one  to  two  weeks  after  they  are  removed  and  all  of  those  show- 
ing an  elevation  of  temperature  should  be  isolated.  By  careful 
isolation  and  safe  disposition  of  the  dead  animals  the  spread  of 
the  disease  can  be  checked.  Animals  do  not,  as  a  rule,  spread 
the  virus  when  the  first  sj^mptom  (rise  of  temperature)  can  be 
detected.  All  infected  stables  and  yards  should  be  thoroughly 
disinfected. 

REFERENCES. 

1.  Chester.  Anthrax,  bacteriological  work.  Report  Del.  Agr. 
£.vpt.  Station.     1S95,  p.  64. 

2.  Chester.  Protective  inoculation  against  anthrax.  Proceedings 
of  the  Society  for  the  Promotion  of  Agricultural  Scieyice.     1896,  p.  52. 

3.  Davaine.  Recherches  sur  les  infusoires  du  sang  dans  la  maladie 
connue  sous  le  nom  de  sang  de  rate.  Comp.  Rend,  dc  V  Acad.  des.  Sc. 
1863.     1864.     1865. 

4.  Dai^rymple.  Anthrax  and  protective  inoculation  in  Louisiana. 
Proceedings  of  the  Am.  Vet.  Med.  Assn.     1901,  p.  147. 


98  INFECTIOUS    LEUKAEMIA 

5.  Koch.  Die  Aetiologie  der  Milzbrand-Krankheit  begriindet  auf 
die  Entwickelungsgeschichte  des  Bacillus  Anthracis.  Cohn's  Bextr.  ~ur 
Biol,  der  Pflanzen.     Bd.  II  ( 1876)  p.  277. 

6.  M'Fadyean.  Anthrax.  The  Jour,  of  Comp.  Path,  and  Therap. 
Vol.  XI.     (189S)  p.  51. 

7.  Moore.  Report  of  an  outbreak  of  Anthrax.  Annual  Report, 
Coinniissioner  of  Agriculture  of  the  State  of  New  York.     1897. 

8.  Pasteur,  Chamberland  ET  Roux.  De  I'attenuation  des  virus 
et  de  leur  retour  a  la  virulence.  Comp.  Rend,  de  V  Acad,  des  Sc.  T.  XCII 
(1881).     p.  427. 

9.  Pasteur.     Le  vaccin  des  charbon.     Ibid.     p.  666. 

10.     PoLLENDER.     Mikroscopische    und    michrochemische  Untersu- 
chung  der  Milzbrandblutes.      1855. 


INFECTIOUS  LEUKAEMIA  IN  FOWLS. 

§  82.  Characterization.  A  specific  leukaemia  of  fowls 
caused  b}^  a  bacterium.  It  is  not  known  whether  or  not  other 
species  of  domesticated  birds  are  susceptible. 

§  83.  History.  This  disease  was  first  briefly  described, 
but  not  named,  by  Moore  in  1895.  At  that  time  it  had  been 
studied  in  but  a  few  fowls  and  these  the  last  to  die  in  their 
respective  flocks.  In  the  following  year  other  fowls  were  ex- 
amined very  carefully  from  two  outbreaks  of  the  disease  and  it 
is  upon  the  data  obtained  in  these  investigations  together  with 
those  procured  from  many  produced  cases  that  the  description 
of  the  disease  is  based.  In  1898,  Dawson  found  it  to  be  the 
cause  of  very  serious  losses  among  poultry  near  Baltimore,  Md. 
In  all  of  the  outbreaks  studied,  the  owners  of  the  fowls  first 
reported  the  disease  as  chicken  cholera. 

§  84.  Geographical  distribution.  It  was  first  studied 
in  fowls  taken  from  an  outbreak  in  Virginia.  Since  then,  it 
has  been  identified  in  Maryland,  the  District  of  Columbia,  and 
Block  Island,  R.  I.  There  is  good  evidence  in  the  numerous 
reports  of  destructive  fowl  disease  to  believe  that  it  is  quite 
widespread  in  the  United  States.  Thus  far,  there  seem  to  be 
no  reports  of  its  existence  in  other  countries. 


ETIOLOGY 


99 


§  85.  Etiology.  Moore  isolated  and  described  a  patho- 
genic bacterium  which  he  designated  Badermmsangtmiarmm. 
With    this     oraranism     the 


disease  has  been  produced 
in  health}-  fowls  both  by 
feeding  cultures  and  by  in- 
travenous injections.  Its 
etiological  relation  to  the 
disease  is,  therefore,  quite 
clearly  established.  It  is 
possible  that  certain  accom- 
panying conditions  may  be 
necessary  in  conjunction 
with  the  organism  to  cause 


0 


0 


Fig.  13.     Bacterium  sanguinarium. 


the  disease  to  spread  rapidly  in  a  flock.  Experimentally  it 
did  not  spread  from  diseased  (inoculated  or  fed)  to  healthy 
fowls  when  kept  in  the  same  yard. 


Fig.  14.  A  cluDip  of  Bad.  sanguinarium  in  a  blood  space  in  the  liver. 
(a)  Bacteria,  {b)  red  blood  corpuscles,  [c)  liver  cells  {much  enlarged). 

^86.  Symptoms.  From  the  statement  of  the  owners  of 
the  diseased  fowls  in  the  different  outbreaks  and  from  the  ap- 
pearance of  those  in  which  the  disease  was  artificially  pro- 


lOO 


INFECTIOUS    LEUKAEMIA 


duced,  little  can  be  positively  stated  concerning  the  early 
symptoms.  There  is  a  pronounced  anaemic  condition  of  the 
mucosa  of  the  head.  An  examination  of  the  blood  shows  a 
marked  diminution  in  the  number  of  red  corpuscles  and  an 
increase  in  the  number  of  white  ones.  In  the  disease  pro- 
duced artificially  by  feeding  cultures  of  the  specific  organism 
there  is,  in  most  cases,  a  marked  drowsiness  and  general 
debility  manifested  from  one  to  four  days  before  death  occurs. 
The  period  during  which  the  prostration  continues  varies 
from  a  few  hours  to  two  days.  The  mucous  membranes  and 
skin  about  the  head  become  pale.  There  is  an  elevation  of 
from  I  to  4  degrees  of  temperature.  The  fever  is  of  a  con- 
tinuous type,  as  shown  in  the  appended  temperature  chart  of 
two  fowls  in  which  the  disease  was  produced  artificially  : 


FAHR 

Hi 

III 

I/O 
101 
106 

107 

lOh 


/3 


1 

\ 

_. 

-  — *-- 

^^ 

^  *^ 

,D« 

ad. 

/    'v 

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^-^ 

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_  -  - 

---' 

/°' 

dd. 

V'' 

' 

^ 

^ 

1 

/^ 

^  / 

■J 

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--■^» 

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.--'  / 

1 

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k^^~" 

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3  -  - 

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Fig.  15.     Temperature  chart  of  tivo  cases  of  infectious  leukaemia 
artificially  produced  in  fowls. 

Although  the  course  of  the  disease  in  different  fowls  is 
usually  constant,  there  are  many  variations.  The  time  re- 
quired for  fatal  results  is  from  two  to  three  weeks,  but  ordinarily 
death  occur  in  about  eight  days  after  feeding  the  cultures.  The 
rise  in  temperature  can  be  detected  about  the  third  day  and  ex- 
ternal symptoms  about  the  fifth  or  sixth,  occasionally  not  until 
a  few  hours  before  death.  The  symptoms  observed  in  the 
cases  produced  by  feeding  correspond  with  those  described  by 
the  owners  of  affected  flocks. 

As  indicated  in  the  inoculation  experiments,  the  symp- 
toms following  the  intravenous  injection  of  the  virus  were,    as 


MORBID    ANATOMY  lOI 

would  be  expected,  considerably  modified  from  those  in  fowls 
which  contracted  the  disease  by  the  ingestion  of  cultures  of 
the  specific  bacterium. 

i:;  87.  Morbid  anatomy.  The  only  constant  lesions 
found  in  the  fowls  which  contract  the  disease  naturally,  as 
well  as  in  those  fed  upon  the  virus,  are  in  the  liver  and  blood. 
The  liver  is  somewhat  enlarged  and  dark  colored.  A  close  in- 
spection shows  the  surface  to  be  sprinkled  with  minute  grayish 
areas.  The  microscopic  examination  shows  the  blood  spaces 
to  be  distended.  The  hepatic  cells  are  frequently  changed,  so 
that  the}^  stain  very  feebh',  and  not  infrequently  the  cells  are 
isolated  and  their  outlines  indistinct.  Occasionally  foci  are 
observed  in  which  the  liver  cells  appear  to  be  dead  and  the  in- 
tervening spaces  infiltrated  with  round  cells.  The  changes  in 
the  hepatic  tissue  are  presumably  secondary  to  the  engorge- 
ment of  the  organ  with  blood. 

The  rareness  with  which  the  intestinal  tract  is  affected  in 
both  the  natural  and  artificially  produced  cases  is  exceedingly 
interesting  and  important  for  the  differential  diagnosis.  There 
is  in  most  cases  a  hypersemia  of  the  mucous  membrane  of  the 
colon,  but  this  condition  is  not  uncommon  in  the  health}'  indi- 
vidual. The  kidneys  are  generally  but  not  uniformly  pale. 
They  are  streaked  with  reddish  lines,  due  to  the  injection  of 
blood  vessels.  In  section  the  tubular  epithelium  appears  to  be 
normal.  The  kidneys  seem  to  be,  from  the  number  of  bacteria 
in  the  cover-glass  preparations,  especially  favorable  for  the 
localization  of  the  specific  organism.  The  spleen  is  rarely  dis- 
colored or  engorged  with  blood.  The  lymphatic  glands  are 
not  appreciably  enlarged  in  any  individual  examined.  The 
lungs  except  in  chronic  cases  are  normal.  The  heart  muscle 
is  usually  pale  and  sprinkled  with  grayish  points,  due  to  cell 
infiltration  and  necrosis.  These  lesions  are  so  common  that  it 
seems  safe  to  consider  them  characteristic  manifestations. 
Death  usually  occurrs  in  systole,  the  auricles  containing  very 
little  thin,  unclotted  blood.  The  brain  and  spinal  cord  are 
unaffected. 

The  most  important  alterations  are  found  in  the  blood. 
These  consist  of  the  gradual    disappearance  of  the   red    cor- 


I02 


INFECTIOUS    LEUKAEMIA 


puscles  and  increase  in  the  number  of  white  ones,  as  deter- 
mined by  blood  counts  made  daih'  or  ever}-  other  da}-,  from 
the  time  of  inoculation  or  of  feeding  the  virus  until  the  day  of 
death. 

The  diminution  in  the  number  of  red  corpuscles  and  the  in- 
crease in  the  number  of  white  ones  are  illustrated  in  the  blood 
coimt  of  two  cases  of  artificialh'  produced  disease,  (p.  105). 
In  carefully  heated  cover-glass  preparations  of  healthy 
fowl  blood  stained  with  methylene-blue  and  eosin,  the  nuclei 
are  colored  a  deep  blue,  and  the  cellular  protoplasm  surround- 
ing the  nucleus  is  stained  by  the  eosin.  In  similar  prepara- 
tions made  from  the  blood   of  the   affected   fowls  there   are  a 

greater  or  less  number  of 
corpuscles  which  do  not 
take  the  eosin  stain.  In 
these  the  portion  of  the 
corpuscle  surrounding  the 
nucleus  remains  unstained 
or  becomes  slightly  tinted 
with  blue.  It  occasionally 
contains  one  or  more  vacu- 
oles, and  the  margin  is  fre- 
quently broken.  In  some  in- 
stances a  considerable  por- 
tion of  the  corpuscle  has 
disappeared,  leaving  a  few 
free  nuclei.  The  apparent 
dissolving  away  of  the  red 
corpuscles  has  been  fre- 
quently observed,  and  cor- 
puscles showing  the  inter- 
mediate stages  are  readily  detected  in  carefully  prepared 
specimens. 

The  cause  of  the  destruction  of  the  red  corpuscles  is  not 
yet  satisfactorily  explained.  In  his  report  on  fowl  cholera, 
Salmon  illustrates  leucocytes  surrounding  the  red  corpuscles, 
but  the  marked  diminution  of  the  red  cells  was  not  deter- 
mined.   He  speaks,  however,  of  the  pale  color  of  the  blood.    In 


Fig.  16.  Blood  from  a  well  ad- 
vanced case  of  infectious  leukaemia 
showing  changes  in  red  corpuscles  and 
increase  in  number  of  leucocytes. 


MORBID    ANATOMY 


lO- 


fresh  preparations  of  the  blood,  portions  of  red  cells  may  be 
seen  within  the  granular  leucocytes.  The  determination  of  the 
extent  of  this  mode  of  destruction  of  the  red  corpuscles  neces- 
sitates further  investigation. 

T.\BLE   SHOWING   CHANGES   IN   THE    NUMBER   OF   CORPUSCLES. 


Fowl  No.  82,  inoculated  in  the  wing  vein,  February  6. 


Date 


Feb.    6 
7 

8 

9 
II 

13 

14 


Tempera- 
ture (°F.) 


107.4 

109 

108.2 

108.4 

107.4 

110.2 

108 


Number  of 

Number  of 

red  cor- 

white cor- 

puscles 

puscles 

per  c.  mm. 

perc.  mm. 

3,744,444 

21,222 

3.417.391 

26,087 

2,784,700 

55.000 

2,807,692 

76,925 

3,481,818 

90,909 

2,133.333 

100,000 

2,530,000 

140,000 

Remarks 


Well. 
Apparently  well. 

Do. 

Do. 
Feathers  ruffled  ;  refuses  food. 
Very  quiet  ;  comb  pale. 
Fowl  died  later  in  the  day. 


Fowl  No 

.  501,  fed 

culture  March  26. 

Date 

Tempera- 
ture (°F.) 

Number  of 
red  cor- 
puscles 

per  c.  mm. 

Number  of 
white  cor- 

pu.scles 
per  c,  mm. 

Remarks. 

Mar.  26 

2S 

Apr.    2 
3 

4 

106.2 
110 
110.6 
106 

3,534,000 
2,430,000 
1,684,210 
1,745,000 

18,940 

70,000 

80,000 

245.432 

Well. 

Fowl  eats  very  little. 

Blood  very  pale  ;  fowl  weak  ;  refuses  food. 
Very   wea'k ;      many    red    corpuscles     at- 
.    tacked  by  leucocytes. 
Found  dead. 

In  fresh  preparations  of 
the  blood  of  affected  fowls 
examined  in  Toisson's  fluid, 
red  corpuscles  which  take 
the  violet  stain  more  or  less 
intensely  throughout  are 
frequently  observed. 

In  the  blood  of  poultry 
two  distinct  classes  of  white 
corpuscles  are  conspicuous. 
The  first  which  predomin- 
ates in  numbers,  contains 
from  one  to  four  nuclei,  and 
the  cytoplasm  is  sprinkled 
with  a  variable  number  of 
round,  elongated,  or  spin- 
dle-shaped bodies.  In  the 
fresh    condition     they    are 


w 


Fig.  17.     Section  of  chicken's  liver 
showing  engorgement  of  blood. 


I04 


IXFECTIOrs    LEUKAEMIA 


highly  refractory.  They  stain  with  eosin,  and  if  the  prepara- 
tions are  heated  sufficiently  they  will  retain  certain  of  the  aniline 
dyes.  The  other  class  consists  of  round  or  nearly  round  cells 
which  take  the  blue  stain  feebly.  Usually  it  is  difficult  to  detect 
the  nucleus,  although  it  is  occasionally  distinct.  Between  these 
two  types  there  are  many  varieties.  The  leucocytes  containing 
the  spindle-shaped  bodies  appear  to  be  the  phagocytes  as  they 
were  the  only  ones  which  were  observed  to  attack  the  red  cor- 
puscles. Bacteria  have  not  been  demonstrated  in  these  cells, 
although  their  presence  has,  in  several  cases,  been  suspected. 
From  the  appearances  observed  in  the  red  blood  corpuscles  it 


Fig.  i8.  The  phagocytic  action  of  the  white  blood  corpuscles  upon 
the  red  ones  in  case  of  advanced  leukaemia.  The  changes  represented 
from  I  tog  took  place  in  jj  minutes. 

seems  highly  probable  that  phagocytosis  plays  a  comparatively 
large  part  in  their  destruction.  Another  hypothesis  is  also  sug- 
gested, namely,  that  a  toxin  produced  during  the  multiplica- 
tion of  the  specific  organism  has  this  effect  on  the  red  corpuscles. 
In  the  fresh  preparations  we  can  observe  the  phagocytes  attack- 
ing the  red  cells.  In  the  stained  ones  mutilated  red  corpuscles 
and  free  nuclei  are  present.  The  hypothesis  is  suggested  that 
the  leucocytes  partially  digest  certain  of  the  red  corpuscles  in 
their  attack  upon  them.  Whether  these  changes  are  entirely 
attributable  to  the  phagocytes  is  still  an  open  question. 


DIFFERENTIAL    DIAGNOSIS 


105 


In  the  blood  from  healthy  fowls  it  is  coraparativeh'  rare  to- 
see  one  of  the  white  corpuscles  attacking  a  red  one.  As  the 
disease  progresses,  however,  this  warfare  becomes  very  con- 
spicuous, owing  perhaps  to  the  increased  number  of  the  color- 
less cells.  Up  to  the  present  the  study  of  these  corpuscles  has 
not  been  extended  beyond  the  observation  of  the  general  ap- 
pearance of  these  structures,  and  no  attempt  is  made  to  explain 
the  apparently  marvelous  increase  in  the  number  of  the  leuco- 
cytes. It  is  an  interesting  and  as  j^et  unexplained  fact  that 
the  increase  in  the  white  corpuscles  is  apparently  restricted  to 
those  containing  the  spindle-shaped  bodies. 

§  88.  Differential  diagnosis.  Intestinal  disturbances, 
especially  diarrhoea  and  fowl  cholera,  are  the  diseases  liable  to 
be  mistaken  for  infectious  leukaemia. 

A  comparison  of  the  important  changes  in  the  morbid 
anatomy  in  fowl  cholera  as  described  by  European  writers 
and  in  the  disease  under  consideration  can  be  made  from  the 
appended  columns,  in  which  their  more  characteristic  lesions 
are  contrasted  : 


Lesions  in  Foivl  cholera. 

1.  Duration  of  the  disease  from  a 

few  hours  to  several  days. 

2.  Elevation  of  temperature. 

3.  Diarrhoea. 

4.  Intestines  deeply  reddened. 

5.  Intestinal      contents      liquid, 

mucopurulent,     or    blood 
stained. 

6.  Heart     dotted     with     ecchy- 

moses. 

7.  Lungs  affected,  hyperaemic  or 

pneumonic. 

8.  Specific  organisms  appear  in 

large  numbers  in  the  blood 
and  organs. 

9.  Blood  pale  (cause   not  deter- 

mined). 

ID.     Condition    of   leucocytes    not 
determined. 


Lesions  in  infectious  leukaemia.  '\ 

1.  Duration  of  the  disease  from 

a  few  hours  to  several  daj^s. 

2.  Elevation  of  temperature. 

3.  Diarrhoea  very  rare. 

4.  Intestines  pale. 

5.  Intestinal  contents  normal  in 

consistencv. 


6. 


7- 


•9 


10. 


Heart  usually  pale  and  dotted 
with  grayish  points,  due 
to  cell  infiltration. 

Lungs  normal,  excepting  in 
modified  cases. 

Specific  organisms  compara- 
tively few  in  the  blood 
and  organs. 

Blood  pale,  marked  diminu- 
tion in  the  number  of  red 
corpuscles. 

Increase  in  the  number  of 
leucocytes. 


lot) 


INFECTIOUS   LEUKAEMIA 


Attention  should  be  called  to  the  fact  that  as  yet  there 
seems  not  to  have  been  a  careful  study  of  the  condition  of  the 
blood  in  fowl  cholera.  Salmon  observed  many  changes  in  this 
fluid  which  may  have  been  similar  to  or  identical  with  those 
herein  recorded. 

The  difference  betvi'een  the  specific  organism  of  these  two 
diseases  can  be  readily  appreciated  by  a  comparison  of  the 
more  diagnostic  properties  of  each  ;  they  are  arranged  in  par- 
allel columns,  as  follows  : 


Bacterium  of  fowl  cholera. 

1.  Bacterium    short,    with    oval 

ends. 

2.  It  usually    appears   singly   in 

tissues. 

3.  Ordinarily  it  exhiVjits  a  polar 

stain.     (From  tissue. ) 


4.  Grows  feebly  or  not  at  all  on 

gelatin. 

5.  It  does  not  change  milk. 

6.  Resists   drying   from   one    to 

three  da}'s. 

7.  Kills  rabbits   inoculated  sub- 

cutaneously  in  from  eigh- 
teen to  twenty-four  hours. 


8.  It  kills  fowls  when  injected 
subcutaneously  in  small 
quantities. 


5- 
6. 


Bacterium  satiguhiai-ium. 

Bacterium  short,  with  ends 
oval  or  more  pointed. 

It  usualh'  appears  in  pairs 
united  end  to  end  or  in 
clumps  in  tissues. 

It  gives  a  light  center,  with 
uniformly  stained  peri- 
phery. (From  tissue.) 
Rarely  a  polar  stain  is 
observable. 

Decided  growth  on  alkaline 
gelatin. 

Saponifies  milk. 

Resists  drying  from  eight  to 
twelve  days. 

Kills  rabbits  inoculated  in- 
travenously in  from  three 
to  five  days.  Rabbits  in- 
oculated subcutaneously 
remain  well  or  die  in  from 
six  to  ten  days. 

It  does  not  kill  fowls  when 
injected  subcutaneously 
in  small  quantities. 


While  there  are  many  similarities  in  the  symptomatology 
of  these  two  diseases,  there  are  pronounced  differences  in  the 
morbid  anatomy  and  in  the  specific  microorganisms.  These 
facts  will  render  the  positive  differentiation  dependent  upon  a 
careful  bacteriologic  and  pathologic  examination.  In  fowl 
cholera  the  course  of  the  disease  is  more  rapid  than  in  leu- 
kgemia. 


SWINE    ERYSIPELAS  lOJ 

REFERENCES. 

1.  Dawson.  Infectious  leukaemia.  Annual  Report  of  the  Bureau 
of  Animal  Industry,  U.  S.  Dept.  Agric.     1898. 

2.  Moore.  A  studv  of  a  bacillus  obtained  from  three  outbreaks  of 
fowl  cholera      Bulletin  No.  5,  U.  S.  Bureau  of  Animal  Industry.     1S94. 

3.  Moore.  Infectious  leukaemia  in  fowls— A  bacterial  disease 
frequently  mistaken  for  fowl  cholera.  Annual  Report  of  the  Bureau  of 
Animal  Industry.     1S95-6. 


SWINE  ERYSIPELAS. 

§89.  Characterization.  This  disease,  peculiar  to  swine,- 
is  determined  by  a  rise  of  temperature,  cerebral  disturbances, 
and  pronounced  reddening  of  areas  of  the  skin.  It  is  a  disease 
of  adult  life.  It  is  stated  that  pigs  are  rarely  attacked  under 
three  months  or  over  three  years  of  age.  Lydtin  and  Schot- 
telius  found  some  differences  in  the  degree  of  susceptibility  of 
certain  breeds  of  swine.  The  common  country  pig  was  least 
susceptible.  It  is  known  in  France  as  roiigct  and  in  Germany 
as  Rothlaiif. 

§  90.  History.  This  disease  has  been  known  in  Europe 
for  many  years.  It  has  not  been  positively  identified  in  the 
United  States.  Smith  found  a  bacterium  in  rabbits  inoculated 
with  the  organs  of  pigs  that  had  died  of  an  undetermined  disease 
in  Minnesota,  which  was  either  the  bacterium  of  swine  ery- 
sipelas or  of  mouse  septicaemia.  The  latter  organism  had  been 
recorded  on  two  previous  occasions  from  pigs  in  this  country. 

§  91.  Geographical  distribution.  Swine  erysipelas  is 
an  infectious  disease  which  occurs  enzootically  and  in  epi- 
zootics in  most  of  the  countries  of  Europe.  Like  anthrax, 
erysipelas  is  often  stationary.  It  was  formerly  restricted  in 
Bavaria  to  the  districts  along  the  Danube,  and  was  entirely 
unknown  in  southern  Bavaria  (Kitt).  It  is  stated  that  the 
disease  tends  to  become  enzootic  chiefly  in  valleys  and  low- 
lying  plains  which  have  slow-flowing  streams,  and  heavy, 
damp,  clay  soil  ;  and  that  sandy  and  granite  soils  are  compara- 
tively free  from  it.  It  occurs  chiefly  during  the  months  of 
July,  August  and  September,  although  it  appears  sporadically 
during  the  winter  months. 


108  SWINE    ERYSIPELAS 

^  92.     Etiology.      Loeffler    and   Schiit^  '^   /' .  ^ 

pointed  out  m  18S5  that  svvme  er\-sipelas  was  '\''\':^'/t^    / 

caused  by  a  very  slender  bacterium  i  to  2/<  ^   Ll ^^^'  " 

long  and  o.  3  to  o.  4/^  broad ,  straight  or  slightly 

curved,    ends  not    rounded    and    in  cultures 

often    appearing    in    filaments.       It    is   verv 

1,1,  •  r  ^  Fig.   19.     Bac- 

closely    related    to   the   bacterium   of    mouse  i^-yji^n     of    swine 

septicaemia  described  by  Koch  in  1878.  In  erysipelas. 
Europe  where  the  bacterium  of  mouse  septicaemia  is  quite 
•common  swine  erysipelas  prevails.  In  this  country  the  bac- 
terium of  swine  erysipelas  has  not  been  positively  identified. 
At  three  dift'erent  times  an  organism  resembling  it  has  been 
isolated  from  swine.  There  is  much  uncertainty  concerning 
the  relationship  of  the  bacterium  of  mouse  septicaemia  to  that 
of  this  disease.  Smith  has  suggested  that  possibly  the  bac- 
terium which  has  been  found  in  this  country  may  gain  viru- 
lence sufficient  to  produce  epizootics,  if  such  is  not  already  the 
case.  It  is  exceedingly  important  that  careful  search  be  made 
for  this  organism  in  the  outbreaks  among  swine  where  the 
nature  of  the  disease  is  not  clearly  determined.  House  mice 
and  pigeons  are  susceptible  to  the  bacteria  of  swine  erysipelas. 
Guinea-pigs  and  fowls  are  immune.  Rabbits  suffer  from  ery- 
sipelatous swellings  when  inoculated  subcutaneoirsly  in  the  ear. 
§  93-  Symptoms.  It  is  stated  that  after  a  period  of  in- 
cubation of  at  least  three  days,  the  disease  usually  begins  sud- 
denly and  violentl}-.  The  animal  refuses  food,  makes  efforts 
to  vomit,  has  a  rise  of  temperature,  manifests  severe  nervous 
disturbance,  is  very  weak,  torpid  and  indifferent  to  its  sur- 
roundings. When  approached  it  tries  to  hide  itself  under 
its  bedding.  The  hind  quarters  become  weak  and  paralyzed. 
Muscular  spasms  and  grinding  of  teeth  are  sometimes  observed. 
At  first  there  is  constipation,  the  conjunctiva  is  of  a  dark  red  or 
brownish-red  color,  and  the  e^^elids  are  sometimes  swollen. 
Usually  a  day  or  two  after  the  first  symptoms  develop  or,  per- 
haps, from  the  first  attack,  reddish  spots  appear  on  the 
thin  parts  of  skin,  such  as  the  region  of  the  navel,  lower  surface 
of  the  chest,  perineum,  inner  surface  of  the  thighs,  ears  and 
throat.     These  spots,  which  at  first  are  bright  red  and  about 


MORBID    ANATOMY  I09 

the  size  of  a  man's  hand,  become,  later  on,  dark  red  or  purple, 
and  soon  unite  into  large  irregularly-shaped  patches.  As  a 
rule,  they  are  neither  painful  to  the  touch  or  prominent,  but 
sometimes  they  show  a  slight  inflammatory  swelling.  The 
skin  of  the  red  spots,  especially  of  the  ears,  may  suffer  from 
an  eruption  of  vesicles  and  may  even  slough.  The  reddening 
of  the  skin  may  be  very  slight  in  severe  cases,  or  may  appear 
only  immediately  before,  or  even  after  death.  Death'  takes 
place  usually  on  the  third  or  fourth  day.  In  the  very  severe 
form,  the  animal  may  die  in  twenty-four  hours,  otherwise  the 
disease  requires  a  week  or  longer  to  run  its  course. 

Jensen  considers  that  this  disease,  instead  of  being  uni- 
form in  its  clinical  aspect,  manifests  itself  in  the  following 
forms,  which  differ  from  each  other  by  well-marked  peculiari- 
ties. He  also  maintains  that  there  may  sometimes  be  tran- 
sitional forms  between  the  respective  varieties  which  he  enu- 
merates. The  forms  recognized  as  varieties  of  this  disease 
but  more  generally  considered  as  distinct  maladies  and  known 
by  different  names  are  as  follows  :  (  i)  true  erysipelas,  (2)  swine 
urticaria,  (3)  erysipelas  without  redness  of  the  skin,  (4)  dif- 
fuse necrotic  erysipelas  of  the  skin,  (5)  endocarditis  of  ery- 
sipelas. Different  forms  of  epizootic  erysipelas  have  also  been 
described  by  Cornevin,  Hess  and  others. 

§  94.  Morbid  anatomy.  In  the  ordinary  form  of  epi- 
zootic erysipelas  there  is  a  septicaemic  condition  without  any 
well  marked  morbid  changes  of  separate  organs.  In  less  acute 
cases  the  septicaemia  may  give  way  to  haemorrhagic  and 
diphtheritic  gastro-enteritis  considerable  swelling  of  the  lym- 
phatic system,  haemorrhagic  or  parenchymatous  nephritis  and 
hepatitis,  acute  swelling  of  the  spleen,  and  myositis.  The 
hemorrhagic  gastro-enteritis  consists  at  first  of  excessive 
inflammation  of  the  mucous  membrane  of  the  stomach 
in  the  region  of  the  fundus.  The  mucosa  shows  a  dark- 
red  discoloration,  which  is  partly  diffuse  and  partly  in 
spots.  The  cells  suffer  from  cloudy  swelling  and  the  mucous 
membrane  is  covered  with  a  viscid  layer  of  mucus  and  may 
have  superficial  scabs.  The  intestinal  mucous  membrane  is 
swollen,  especially  on  the  top  of  the  folds  and  in  the  neighbor- 


no  SWINE   ERYSIPELAS 

hood  of  Peyer's  patches.  It  is  infiltrated  with  blood  and 
sometimes  shows  superficial  scabs.  Less  frequently,  circum- 
scribed parts  of  the  mucosa  of  the  caecum  and  of  the  anterior 
parts  of  the  colon  suffer  from  a  diptheritic  affection. 

The  solitary  follicles  and  Peyer's  patches  appear  as  prom- 
inent raised  patches.  Sometimes  they  are  infiltrated  with 
blood  and  surrounded  by  a  reddish  band.  There  is  ulceration 
and  cicatrisation  of  the  solitary  and  agminated  follicles.  The 
mesenteric  glands  become  more  swollen  than  the  other  glands 
of  the  body,  of  a  dark  red  color,  and  show  softening.  The 
surface  of  fresh  sections  is  dun-colored  with  interspersed  dark- 
red  areas.  The  paraglandular  tissue  is  hyperaemic,  and  infil- 
trated with  blood. 

The  kidneys  are  enlarged,  the  cortex  of  a  grayish-red  and 
the  medullary  portion  of  a  very  dark-red  color.  Frequently 
catarrhal  nephritis  occurs  as  a  complication. 

The  acute  swelling  of  the  spleen  arises  in  consequence  of 
an  acute  hyperaemia  with  an  increase  of  the  cellular  constitu- 
ents of  the  spleen  in  which  case  the  organ  is  enlarged,  but  not 
softened  as  in  anthrax.  The  pulp  is  of  a  purple  color,  moder- 
ately soft  and  free  from  haemorrhages. 

There  is  cloudy  swelling  and  enlargement  of  the  liver. 
The  surface  of  sections  has  a  greyish-brown  color,  and  the 
acini  are  widened.  The  muscles  are  grey  in  color,  soft,  flac- 
cid, watery,  glistening  and  sometimes  they  are  sprinkled  with 
haemorrhages.  They  give  the  general  appearance  of  boiled 
flesh.  The  myocardium  shows  similar  spotted  changes,  and 
haemorrhages  beneath  the  endocardium. 

In  the  abdominal  and  thoracic  cavities  and  pericardium, 
there  may  be  found  small  quantities  of  an  orange-colored, 
clear  fluid,  which  may  be  mixed  with  flaky  coagula.  Puncti- 
form  haemorrhages  often  appear  under  the  serous  membranes, 
especially  on  the  auricles.  Many  English  veterinarians  regard 
the  occurence  of  more  or  less  luxuriant  vegetations  on  the 
valves  of  the  heart  to  be  so  frequent  as  to  be  almost  diagnostic. 
It  would  appear  from  the  literature  that  this  endocarditis  is 
not  nearly  so  common  in  continental  Europe.  Severe  haemorr- 
hages in  the  brain  and  in  the  dorsal  and  lumbar  portions  of 


MORBID    ANATOMY  III 

the  spinal  cord  are  rare.  The  lungs  remain  unchanged,  or  at 
most  exhibit  a  post  mortem  oedema.  By  microscopical  exami- 
nation, the  specific  bacteria  are  found  everywhere  in  the  body, 
especially  in  the  spleen  and  kidneys,  and  to  a  less  extent  in 
the  blood. 

§  95.  Differential  diagnosis.  Swine  erysipelas  is  to  be 
differentiated  from  (i)  hog  cholera  and  swine  plague.  The 
frequent  reddening  of  the  skin  in  these  diseases  together  with 
the  modified  lesions  so  frequently  observed,  may  cause  confu- 
sion. The  bacteriological  examination  will  enable  the  positive 
diagnosis  to  be  made.      (See  hog  cholera  and  swine  plague.) 

(2)  From  anthrax  which  is  very  rare  in  swine.  Here, 
too,  the  bacteriological  examination  discloses  the  true  nature 
of  the  disease. 

(3)  Erythemata  due  to  various  dietary  causes. 

The  significance  of  a  deep  reddening  of  the  skin  about 
the  head,  abdomen  and  thighs  of  pigs  is  not  fully  determined. 
It  is  clear,  however,  that  such  a  condition  often  occurs  in  the 
absence,  so  far  as  present  knowledge  goes,  of  a  specific  infection. 

§96.  Preventive  inoculation,  Pasteur's  protective  in- 
oculation is  at  present  the  chief  prophylactic  means  employed 
against  epizootic  erysipelas.  The  exact  method  of  preparing 
the  inoculation  material  has  not  been  published.  It  is  known 
that  Pasteur's  vaccine  is  obtained  by  passing  the  bacteria 
through  several  generations  of  rabbits  in  succession  and  then 
cultivating  them  in  nutritive  fluid.  The  animals  inoculated  after 
Pasteur's  method  become,  according  to  him,  only  slightly  ill, 
and  acquire  immunity  to  erysipelas.  The  method  of  inocula- 
tion is  as  follows  :  the  pigs  at  the  age  of  nine  to  sixteen  weeks 
are  first  injected  in  the  subcutaneous  connective  tissue  with  a 
weak  vaccine  and  in  ten  or  twelve  days  after  with  a  stronger 
vaccine. 

The  results  of  the  practical  application  of  this  method 
show  that  it  immunizes  to  a  certain  extent  the  inoculated 
animals.  However,  the  risk  of  the  treatment  is  said  not  to  be 
insignificant.  It  is  held  that  the  inoculated  pigs  infect  the 
healthy  and  may  thus  spread  the  disease.  Besides,  the  adop- 
tion of  this  system  renders  the  inoculated  animals  seriously  ill, 


112  SWINE   ERYSIPELAS 

and  according  to  various  European  reports,  is  attended  by 
a  mortalit}'  of  about  4  per  cent  which  it  is  affirmed  exceeds  the 
total  loss  caused  b}-  epizootic  erysipelas  when  allowed  to  run 
its  course  unmolested. 

Metschnikoff  found  that  the  blood  of  immunized  rabbits 
was  antitoxic,  and  Lorenz  maintains  that  the  serum  of  swine 
which  have  recovered  from  swine  erysipelas  is  also  antitoxic, 
and  will  produce  immunity  in  other  animals.  The  treatment 
introduced  by  Lorenz  is  to  inject  the  immunizing  serum  in  the 
proportion  of  i  cc.  to  every  10  kilogrammes  of  the  body  weight 
of  the  animal.  Two  days  afterward  0.5  to  i.o  cc.  of  virulent 
culture  is  injected,  and  after  twelve  days  the  dose  is  doubled. 
Lorenz  inoculated  294  pigs  ;  twelve  were  suffering  from  swine 
erysipelas,  and  of  these  6  recovered  and  6  died. 

REFERENCES. 

1.  Bang.  Ueber  Rothlauf-Endocarditis  bei  Schweinen.  Deutsche 
Zeitschr.f.    Thiermed.     Bd.  XVIII.     (iSgu.     S.   27. 

2.  Jensen.  Die  Aetiologie  des  Nesselfiebers  und  der  diffuse n 
Hautnekrose  des  Schweines.  ^ Deutsche  Zeitschr.  f.  Thiervicd.  (1S92). 
S.  278. 

3.  LoEFFLER.  Experimentelle  Untersuchungen  iiber  Schweiiie- 
Rothlauf       Arheiten    aus   d.    Kaiserlichen    Gesundheitsamte.       Bd.    I. 

(1885).     S.  46. 

4.  Lorenz.  Die  Schutzimfung  gegen  Schweinerothlauf  nut  An- 
wendung  eines  aus  Blutserum  immunisirter  Thiere  hergestelUen  Inip- 
fstoffes.     Deutsche  Zeitschr.  f.  Thiermed.     Bd.  XX.     (1894).     S.  i. 

5.  Lorenz.  Die  Veterinarpolizeiliche  Behandlung  des  Schwein- 
erothlaufes  und  die  Schutzimfung.  Berliner  thierarz.  Wochen.  (1897). 
p.  574. 

6.  Lorenz.  Schutzimfungen  gegen  den  Rothlauf  der  Schweine. 
Ibid.     (1897).     S.  109. 

7.  MoORE.  Mouse  septicaemia  bacilli  in  a  pigs  spleen  -with  some 
observations  on  their  pathogenic  properties.    Jour,  of  Comp.   Med.  and 

Vet.  Archives.     Vol.  XIII.     (1892).     p.  333. 

S.  Pastuer  ET  Thuillier.  La  vaccination  du  rouget  des  pores  a 
I'aide  du  virus  mortel  attenue  de  cette  maladie.  Coniptes  Reudus  Acad, 
des  Sciences      Vol.  XCVII,  1S83.     p.  1163. 

9.  ScHUTz.  Ueber  den  Rothlauf  der  Schweine  und  die  Impfung 
mit  demselben.  Arbeiten  a.  d.  Kaiserlichen  Gesundheitsamte.  Bd.  I. 
(1S85).     S.  56. 

10.  Smith.  An  Examination  of  Pasteur's  Vaccine  for  Rouget. 
Annual  Report  U.  S.  Bureau  of  Animal  Industry.     18S5.     p.  187. 

11.  Smith.  Swine  erysipelas  or  mouse-septicaemia  bacilli  from  an 
outbreak  of  swine  disease'  Annual  Report,  U.  S.  Bureau  of  Animal 
Industry.     1895-96.     p.  166. 


INFECTIOUS    DISEASES  II3 

GLANDERS. 

vj  97.  Characterization.  Glanders  is  one  of  the  most 
important  diseases  of  horses,  asses  and  mules  and  when  trans- 
mitted to  man,  one  of  the  most  fatal  diseases  of  the  human 
species.  It  runs  an  acute  or  chronic  course  attacking  the  lym- 
phatic S3'Stem  more  especially  in  the  upper  air  passages,  lungs, 
or  skin.  The  disease  is  characterized  by  a  strong  tendency  to 
the  formation  of  small  neoplasms  or  nodules  which  are  likeh' 
to  degenerate  into  ulcers  from  which  exude  a  peculiar  sticky 
discharge.  In  the  very  acute  cases  a  considerable  rise  of  tem- 
perature and  general  debility  may  accompany  the  formation  of 
the  lesions.  Glanders  of  the  skin  is  known  as  farcy.  It  is 
known  in  Germany  as  Rotz  or  Rotzkrankheit  and  in  France  as 
morve. 

B3'  direct  inoculation  several  species  of  animals  may  be  in- 
fected. Thus  the  disease  has  been  reported  in  goats,  rabbits, 
sheep,  guinea  pigs,  field  mice,  and  several  of  the  wild  animals, 
especially  those  of  the  cat  tribe.  Swine  and  pigeons  are  very 
slightly  susceptible.  Cattle,  white  mice,  rats  and  domestic 
fowls  seem  to  be  immune. 

§  98.  History.  The  theory  of  the  contagiousness  of  glan- 
ders was  much  doubted  at  the  beginning  of  this  century.  The 
view  taken  at  the  Alfort  \'eterinary  College  was  that  glanders 
might  arise  spontaneously  from  an  attack  of  strangles.  This 
view  was  far  more  widely  accepted  than  the  theor}^  of  its  con- 
tagiousness, which  was  stoutly  supported  b}-  the  Veterinary 
College  of  Lyons.  It  was  not  until  Rayer  (1837)  had  demon- 
strated the  transmissibilit}^  of  glanders  to  man,  and  Chaveau 
(1868)  had  shown  that  the  virus  was  contained  chiefly  in 
the  firm  component  parts  of  the  infective  material,  that  the 
fact  of  the  infectious  nature  of  the  disease  was  accepted. 

The  theory  of  the  spontaneous  origin  of  glanders  was 
widely  accepted  in  Germany.  vSixty  years  ago  it  was  believed 
that  glanders  could  be  produced  by  the  injection  of  pus,  and 
that  strangles  could  develop  into  glanders.  Glanders  was  looked 
upon  as  a  tubercular  disease,  scroiula,  p3'aemia,  diphtheritis, 
general  d^'-scrasia,  and   cachexia,  respectively.     \'irchow  was 


114  GLANDERS 

the  first  to  declare  that  the  nodules  of  glanders  were  independ- 
ent, anatomical  formations,  which  he  placed  under  the  heading 
of  granulation  tumors.  Gerlach  was  the  strong  advocate  for 
the  exclusivel}-  infectious  origin  of  the  disease.  Leisering  ap- 
pears to  have  been  the  first  to  give  an  accurate  description  of 
the  lesions. 

The  first  biological  researches  into  its  nature  were  made 
in  1868  b}'  Zurn  and  Hallier,  who  found  a  fungus  which  the}^ 
believed  to  be  the  cause  of  the  disease.  In  1882,  Loftier  and 
Schiitz  succeeded  in  finding  the  bacterium  of  glanders,  in  culti- 
vating it,  and  in  transmitting  the  disease  to  other  animals  by 
inoculating  them  with  pure  cultures  of  this  organism.  Their 
researches  furnished  the  positive  proof  that  glanders  is  a  spe- 
cific, infectious  disease,  produced  exclusively'  by  Bacterium 
mallei. 

ij  gg.  Geographical  distribution.  Glanders  exists  in 
the  greater  part  of  the  civilized  world.  It  is  more  common  in 
the  temperate  zones,  w^here  traffic  in  horses  is  active.  In  the 
United  States  it  was  largely  confined  to  the  Northern  States 
before  1S61,  but  it  spread  over  the  South  in  connection  with 
the  civil  war.  It  is  said  to  have  entered  Mexico  with  the 
American  cavalry  in  1847.  Similar!}-,  Portugal  is  said  to  have 
been  exempt  until  the  invasion  b}'  Napoleon  in  1797.  Central 
Hindoostan  was  said  to  be  free  from  it  until  the  war  with  Afghan- 
istan in  1S78.  In  all  these  cases,  the  movements  of  cavalr}-, 
artillery  and  of  commissary  trains  were  responsible  for  the 
introduction  of  the  disease  into  new  territory.  In  our  own 
case  the  sale  of  horses  and  mules  at  the  close  of  the  civil  war 
produced  a  very  general  diffusion  of  this  disease  from  which 
the  country  is  still  suffering. 

Insular  places,  especially  if  far  from  the  main  land  and  free 
from  importation  of  horses,  usually  escape.  Thus  glanders  is 
very  rare  in  Iceland  and  in  the  Faroe  islands.  In  Australia, 
Tasmania  and  New  Zealand  it  is  reported  to  be  unknown. 


ETIOLOGY  I  I  5 

§  loo.   Etiology.   Badermrn  fnallei,  the  q       ^ 

specific   cause  of  glanders,  was  discovered     ,.  "  "C*  Cii  ~^ 
and  isolated  in  pure  culture  almost  at  the    0>^:^    ■^-0.;^ 
same    time     (1882)    bv    Loeffier,     Schiitz,     ^^"^\^  'ry'^'  O. 
Israel,   Bouchard,   Charnn,  Weichselbaum,      '  >S^.  n  —  "C" 
Kauzfeld,    and   Kitt.       It  is  found   in    the       '-"^"•i|)>>0o  " 
recent  nodules,   in   the  discharge  from  the         pj^,   20    Bader- 
nostrils,   pus  from  the  specific  ulcers,    and      iimi  mallei. 
occasionally  in  the  blood  of  animals  affected  with  glanders. 

Morphologically  it  is  a  small  organism  with  rounded  or 
pointed  ends.  It  varies  in  breadth  from  o.25/<  to  0.4//  and 
from  1.5//  to  3//  in  length.  It  is  usually  single  but  pairs,  and 
long  filaments,  especially  on  potato  cultures,  are  not  rare.  It 
frequently  breaks  up  into  short,   almo.st  coccus-like  elements. 

It  stains  with  some  difficulty.  Of  the  aniline  colors,  the 
best  results  are  obtained  when  the  aqueous  solutions  of  these 
dyes  when  they  are  made  feebl}'  alkaline.  It  is  decolorized 
by  Gram's  method. 

It  grows  well,  but  slowly  at  the  body  temperature  on 
glycerine  agar,  in  acid-glycerinized  bouillon,  on  blood-serum 
and  on  potato. 

Of  the  test  animals,  guinea-pigs  and  field  mice  are  the 
most  susceptible.  In  guinea-pigs,  subcutaneous  injections  are 
followed  in  four  or  five  days  by  swelling  at  the  point  of  inocu- 
lation and  sloughing  of  the  skin  which  is  followed  by  the 
formation  of  a  chronic,  purulent  ulcer.  The  lymphatic  glands 
become  inflamed  and  symptoms  of  general  infection  develop  in 
from  two  to  four  weeks  ;  the  glands  suppurate  and  in  males 
the  testicles  are  involved.  A  purulent  inflammation  of  the 
joints  may  occur.  The  formation  of  the  specific  ulcers  upon 
the  nasal  mucous  membrane,  which  forms  one  of  the  characters 
of  the  disease  in  the  horse,  rarely  occur  in  the  guinea-pig  as  a 
result  of  inoculation.  The  disease  is  often  prolonged  for 
several  weeks  or  months.  Guinea-pigs  succumb  usually  in 
from  eight  to  ten  days  when  injected  into  the  peritoneal  cavity. 
In  males,  the  testicles  are  invariably  affected. 

§  loi.  Symptoms,  {a)  Acute  glanders.  Acute  gland- 
ers is  common  in  the  ass  and  mule,    but    infrequent    in    the 


Il6  GLANDERS 

horse.  x\fter  a  period  of  incubation  of  from  three  to  five  da^-s 
the  animal  has  a  chill,  elevation  of  temperature,  a  profuse 
muco-purulent  sticky  discharge,  sometimes  mixed  with  blood, 
from  the  nose.  Particles  of  food  arrested  in  the  pharynx 
occasionally  appear  in  the  nasal  discharge.  If  unilateral  the 
margin  of  the  nostril  swells,  the  mucosa  is  dark-red,  infil- 
trated, marked  with  pea-like,  yellowish  elevations  with  red 
areolae,  which  in  a  few  days  become  eroded,  thus  forming 
spreading  ulcers.  The  submaxillary  lymphatic  glands  on  the 
affected  side  become  enlarged.  There  may,  however,  be  a 
uniform  swelling  filling  the  whole  intermaxillary  space.  The 
course  is  rapid  and  death  ensues,  usually  from  suffocation,  in 
from  the  sixth  to  the  fifteenth  day.  The  acute  form  rarely  if 
ever  becomes  chronic. 

(b).  Chronic  glanders.  In  the  horse,  this  form  of  the 
disease  may  begin  with  a  chill  but  usually  the  onset  is  very 
insidious.  There  may  be  a  muco-purulent,  sticky  discharge 
sometimes  streaked  with  blood  from  one  or  both  nostrils. 
There  may  be  intermittent  or  continued  lameness,  arthritis, 
oedema  of  a  limb,  swelling  of  a  testicle,  cough,  or  epistaxis. 
There  is  usually  a  nodular  but  comparatively  painless  swelling 
of  the  submaxillary  lymph  gland,  on  the  affected  side.  On 
palpation  the  swelling  imparts  a  sensation  suggestive  of  a  num- 
ber of  peas.  They  are  adherent  to  the  adjacent  structures. 
The  nasal  mucosa  is  congested,  of  a  dark  reddish  color  and 
sprinkled  with  superficial  or  deep  ulcers  either  clean  or  covered 
with  crusts. 

Rarely  the  submaxillary  glands  only  are  apparently  dis- 
eased. In  other  cases,  there  is  only  a  cough,  the  latent  lesions 
being  confined  to  the  lungs.  In  still  other  cases,  the  lesions  are 
restricted  to  one  or  both  testicles,  the  spleen,  or  some  other 
internal  organ,  and  symptoms  may  or  may  not  be  present. 
Chronic  glanders  frequently  terminates  in  the  acute  form. 

In  chronic  cutaneous  glanders,  with  or  without  oedema  of 
the  limbs,  there  may  be  one  or  many  nodules  on  the  fetlock, 
or  elsewhere  on  the  line  of  the  lymphatic  vessels,  with  indura- 
tion of  the  lymphatics  extending  from  it.  The  nodules  may 
be  suppurating  and  discharging,  or  they  may  be  closed. 


MORBID    ANATOMY  II7 

^  102.  Morbid  anatomy.  In  chronic  glanders,  the  most 
frequent  locations  of  the  lesions  are  on  the  respirator}-  mucous 
membrane,  in  the  lungs,  lymph  glands  and  skin.  Other  or- 
gans are  more  rarely  invaded.  The  upper  respiratory  mucous 
membrane  is  the  usual  seat  of  the  lesions.     Glanders  occurs  in  y 

two  forms,  viz.,    (a)  as  circumscribed   nodules  with  the  forma-   cA  ^y-*''^^ 
tion  of  ulcers   and  cicatrices;  and  (d)  as  diffuse  or  infiltrated      ^'\ 
lesions. 

(a)  In  nodular  glanders,  which  is  the  common  form,  the 
lesions  ar.e  most  frequently  situated  on  the  upper  portion  of 
the  nasal  septum,  and  in  the  cavities  of  the  turbinated  bones. 
The  affection  begins  with  the  appearance  of  nodules  varying 
in  size  from  a  grain  of  sand  to  a  millet  seed.  They  are  more 
or  less  translucent,  of  a  roundish  or  oval  shape,  and  of  a  dirty 
gray  or  grayish  red  color.  The  nodules,  w^hich  may  attahi  to 
the  maximum  size  of  a  pea,  project  somewhat  above  the  sur- 
face of  the  mucous  membrane.  They  are  surrounded  by  a  red- 
dish ring.  Some  of  them  are  i.solated  and  others  are  arranged  in 
groups.  Microscopically  they  consist  of  a  large  number  of  lym- 
phoid cells,  which  disintegrate  in  the  centre  of  the  nodule.  In 
consequence  of  the  central  fatty  and  purulent  disintegration,  the 
nodules  become  yellowish  in  color,  discharge  and  form  ulcers. 
These  ulcers  are  sometimes  superficial,  sometimes  deep,  lentic- 
ular or  crateriform,  surrounded  by  a  hard,  indurated  edge,  and 
frequently  becoming  confluent  with  irregularly  serrated  and 
eroded  edges.  They  are  sometimes  covered  with  a  brownish 
crust.  The  ulcers  may  increase  in  area  or  in  depth  and  may 
even  involve  the  underlying  cartilage  or  bone,  causing  perfora- 
tion of  the  septum  nasi,  and  distensions  of  the  maxillary  or  exos- 
toses on  the  turbinated  bones.  The  shallow  lenticular  ulcers 
may  heal  without  leaving  any  visible  changes  ;  but  the  deeper 
ones,  after  granulating,  leave  a  radiating,  star-shaped  cicatrix 
which  is  either  smooth  or  horny,  and  which,  according  to  the 
shape  of  the  ulcer,  may  be  of  an  irregular,  oblong  form.  The 
nasal  septum  is  frequently  covered  with  these  scars.  The 
ulcers  and  cicatrices  are  sometimes  found  in  the  maxillary  and 
frontal  sinuses,  in  the  guttural  pouches  and  in  the  eustachian 
tubes.     They  may  also  occur  in  the  larynx,  especially  in  the  re- 


/    ; 


ii8 


GIvANDERS 


t 


Fig.  21.     Photograph  of  a  portion  of  a  nasal  septum  showing  ulcers 
in  advanced  glanders,     [a)  Perforations  of  septuju. 

gion  of  the  lower  vocal  chords.  In  the  trachea  and  even  in  the 
bronchi,  particularly  on  the  anterior  surface,  numerous  long, 
oval  ulcers  or  long,  pointed,  serrated  scars  are  frequently  found. 
In  addition  to  the  ulcers,  a  catarrhal  inflammation  of  the 
mucous  membrane  is  very  apt  to  be  present. 


MORBID    ANATOMY  I  I9 

Diffuse  glanders  manifests  itself  as  a  diffuse  catarrh  of  the 
mucous  membrane  of  the  nasal  and  neighboring  cavities  with 
superficial  ulceration,  thrombosis  of  the  veins,  inflammatory 
infiltration  of  the  submucosa,  considerable  thickening  of  the 
mucous  membrane  and  the  formation  of  a  peculiar,  radiating 
cicatrix. 

The  nodular  and  infiltrated  forms  are  found   in  the  lungs. 

In  the  nodular  form  the  lungs  contain  nodules*  varying  in 
size  from  a  millet  seed  to  that  of  a  pea.  They  are  gray  by 
transmitted  light,  glassy  and  pearl  gray  by  reflected  light,  and 
are  surrounded  by  a  hemorrhagic  ring.  The  center  of  the 
nodules  shows  a  pale  yellow  point  in  consequence  of  caseation 
and  disintegration  of  the  innermost  cells.  These  nodules  are 
of  different  sizes,  of  varying  numbers,  and  of  different  ages. 
The  formation  of  a  capsule  by  a  connective  tissue  membrane  is 
induced  by  a  reactive  inflammation  in  the  tissue  surrounding 
the  nodule.  The  nodules  ma}-  be  of  an  embolic  origin,  situ- 
ated principally  in  the  periphery  of  the  lung,  their  structure 
being  the  same  as  that  of  the  nodules  on  the  nasal  mucosa. 
Sometimes  the  lung  nodules  represent  lobular  pneumonic  foci,  in 
which  the  alveoli  are  filled  with  red  and  white  blood  corpus- 
cles and  with  desquamated  epithelium  of  the  lungs.  Central 
disintegration  occurs  very  early.  These  areas  are  surrounded 
by  a  membrane  resulting  from  a  reactive  inflammation  which 
manifests  itself  and  out  of  which  a  connective  tissue  capsule 
develops  later  on.  In  other  cases,  the  foci  suppurate  forming 
cavities.  Besides  these  nodules,  there  are  often  chronic  bron- 
chitis, peribronchitis,  parabronchitis,  atelectasis,  inflammation 
of  the  tissue  of  the  lung  and  less  frequently  circumscribed  or 
■exudative  pleuritis. 

Infiltrated  glanders  of  the  lungs  form  tumors  from  the  .size 
of  a  walnut   to   that   of   a   child's  head,  consisting  of  a  diffuse 


*Nocard  points  out  that  when  glandered  horses  are  treated  with  mal- 
lein,  a  certain  proportion  of  them  recover  in  which  case  nodules  that  were 
present  in  the  lungs  cease  to  contain  living  bacteria,  a  fact  he  has  fully 
proved  by  inoculation.  On  post-mortem  examination  the  nodules  may 
be  readily  felt  by  passing  the  hand  with  firm  pressure  over  the  surface 
of  the  lung  which,  when  badly  diseased,  will  feel  like  a  bag  full  of  shot 
or  peas. 


I20 


GLANDERS 


glanderous  infiltration  of  the  alveoli  and  of  the  interstitial  con- 
nective tissue.  Frequently  on  section  the  infiltrated  parts  of 
the  lungs  resemble  ver^-  closel}'  a  soft  sarcoma.  They  are  of  a 
dirty  white  color,  of  a  gelatinous,  juicy  consistence,  and  irreg- 
ular in  shape.  They  may  either  become  indurated  so  as  to 
form  hard,  connective  tissue  like  new  growths  (fibroma-like 
tumors  of  glanders,  according  to  Gerlach),  or  they  may  become 
gangrenous.  In  nodular  and  in  infiltrated  glanders  of  the 
lungs,  the  bronchial  glands,  and  frequently  the  mediastinal 
glands  become  enlarged,  indurated  and  studded  with  small 
foci  of  cell  infiltration. 

In  glanders  of  the 
skin  (farcy)  the  nod- 
ules are  found  in  the 
papillary  layer,  in  the 
cutis  and  in  the  sub- 
cutaneous and  super- 
ficial intermuscular 
tissue.  The  cutane- 
ous nodules  var}-  in 
size  from  a  hemp  seed 
up  to  that  of  a  pea. 
They  suppurate  rapid- 
ly and  form  small 
ulcers.  The  nodules 
in  the  subcutis  are  in- 
flammatory (metasta- 
tic) tumors  from  the 
size  of  a  pea  to  that  of 
a  hen's  egg.  The^^ 
change  into  large  ab- 
scesses and  discharge 
externall}'.  In  the  re- 
gion of  the  nodules 
the  lymphatic  vessels 
are  inflamed,  swollen, 

and  frequentlv  resem- 
FiG.  22.    Photos^raph  shoivins:  farcy  buds    ,  ,  '  , 

,     ,  1     ^    \  ble  a  rosary  or  knotted 

{cutaneous  glanders).  ■' 


GI.ANDERS    IN    MAN  121 

cord.  Ulcers  often  develop  from  these  secondar}-  nodes.  The 
neighboring  lymph  glands  are  at  first  swollen  and  soft,  but 
later  they  become  indurated  by  the  growth  of  connective  tissue 
and  studded  with  dirty  white  nodules  about  as  large  as  a  pin's 
head,  or  with  yellow  foci  of  caseation.  The  capsule  around 
the  lymph  glands  becomes  infiltrated  with  small  cells  and  sub- 
sequently thickened.  In  rare  cases  secondar}-  chronic  farcy 
occurs.  It  is  marked  by  a  large  diffuse  new-growth  of  con- 
nective tissue  with  nodular  thickening  of  the  skin.  This  con- 
dition is  termed  glanderous  elephantiasis  or  pachyderma.  It 
chiefly  affects  the  limbs  and  head. 

Of  the  abdominal  organs,  the  spleen  is  most  frequently  at- 
tacked. It  then  contains  embolic  nodules,  varying  in  size 
and  which  either  suppurate,  or  become  calcareous.  Similar 
nodules  occur,  though  not  so  often,  in  the  liver,  kidneys,  testi- 
cles, brain,  muscles,  heart,  and  bones.  In  the  bones,  a  cellu- 
lar infiltration  of  the  medulla  and  purulent  breaking  down  of 
the  osseous  tissue.  Ulcers  are  ver}'  rare  on  the  mucous  mem- 
branes of  the  eyes,  stomach  and  vagina.  The  blood  shows 
signs  of  slight  leucocytosis.  The  specific  bacteria  are  found 
in  the  blood  only  in  cases  of  acute  general  infection. 

The  anatomical  changes  in  acute  glanders  consist  chiefl}' 
in  a  disintegration  of  the  respirator}-  mucous  membrane,  in  a 
serous  infiltration  of  the  submucous,  subcutis,  and  inter- 
muscular tissue,  with  inflammation  and  suppuration  of  the 
Ij-mph  vessels  and  lymph  glands.  There  are  also  metastatic 
formations  in  the  skin  and  lungs.  The  nasal  mucous  mem- 
branes are  covered  with  rapidly  spreading  ulcers  with  consider- 
able infiltration  into  the  submucosa.  The  mucous  membrane 
of  the  larynx  and  pharynx  is  swollen  and  covered  with  ulcers. 
The  lungs  are  studded  with  purulent  metastatic  foci  or  fresh 
nodules.  The  skin  is  excessively  swollen  and  covered  with 
glanderous  nodes.  Sometimes  diffuse  gangrene  of  the  skin 
occurs. 

§  103.  Glanders  in  man.  The  symptoms  of  glanders 
in  man  are  of  much  importance  to  the  veterinary  surgeon. 
Although  the  susceptibility  to  the  disease  is  usuallj'  not  very 
great,  cases  of  human  glanders  unfortunately  occur,  especially 


122  GLANDERS 

among'  veterinary  surgeons  and  those  having  the  care  of 
horses.  Human  glanders  is  reported  to  be  quite  common  in 
Russia.  The  parts  usually  first  affected  are  the  hands,  nasal 
mucous  membrane,  lips  and  conjunctiva.  After  a  period  of 
incubation  of  from  three  to  five  days  the  infected  part  becomes 
swollen  and  painful,  with  subsequent  inflammation  of  the 
lymph  vessels  and  swelling  of  the  glands.  Fever  is  often  the 
first  symptom,  and  it  is  nearly  always  followed  by  a  nasal  dis- 
charge ;  ulcers  on  the  nasal  mucous  membrane,  pustules  and 
abscesses  in  the  skin,  ulcers  in  the  oral  cavity,  larynx,  and 
conjunctiva,  articular  swellings,  and  grave  general  distur- 
bances. Sometimes  there  is  intense  gastro-intestinal  trotible. 
Nodules  occur  in  the  lungs  in  some  cases.  As  a  rule,  death 
takes  place  in  from  two  to  four  weeks,  and  occasionally  in  a  few 
days.  In  other  instances,  the  disease  becomes  chronic,  with  a 
duration  of  months  or  3'ears.  Bad.  mallei  have  been  found  in 
the  blood  in  cases  of  acute  glanders.  The  positive  diagnosis 
depends  on  the  possibility  of  infection  having  taken  place,  on 
inoculation  in  guinea-pigs,  or  the  proof  of  the  presence  of 
Bad.  viallei.  Treatment  is  usualh'  of  no  avail.  The  only 
hopeful  cases  are  those  that  are  purely  local  in  their  manifesta- 
tion. A  few  of  these  are  reported  to  have  been  cured  by 
applying  deep  cauterization. 

104.  Differential  diagnosis.  Glanders  is  to  be  differ- 
entiated from  a  variety  of  nasal  and  lymphatic  disorders  more 
or  less  common  in  the  horse  kind.  Before  the  discovery  of 
the  specific  bacterittm  of  glanders  or  of  mallein,  it  was  neces- 
sary to  determine  as  closely  as  possible  the  differential  anato- 
mical characters  between  glanders  and  those  of  other  affec- 
tions, such  as  chronic  nasal  catarrh,  strangles,  lymphangitis, 
follicular  ulceration  of  the  nasal  mucosa,  cancer,  sarcoma, 
actinomycosis,  melanosis  and  the  like.  Since  the  discovery  of 
practically  a  positive  means  of  diagnosis,  it  does  not  seem  wise 
to  speculate  upon  the  chances  of  the  correct  differential  diag- 
nosis by  former  methods.  If  the  diagnosis  can  not  be  made 
from  the  manifestations  of  the  disease,  two  reliable  courses  are 
possible  although  in  most  cases,  but  one  (mallein)  is  to  be 
recommended.  These  are  (i)  animal  inoculation,  and  (2)  the 
use  of  mallein. 


DIFFERENTIAL    DIAGNOSIS  I  23 

(i).  Animal  inoculation.  Male  guinea-pigs  should  be 
used.  The  material  for  inoculation  usually  consists  of  the 
nasal  discharge  from  the  suspected  glandered  horse,  bits  of 
scrapings  from  the  ulcers,  or  pieces  of  other  diseased  tissue. 
The  method  to  be  followed  is  precisely  the  same  as  with  the 
subcutaneous  inoculation  of  tuberculous  material.  In  these 
cases  there  is  liable  to  be  a  local  swelling  and  abscess.  The 
first  symptom  of  glanders  noticed  is  usually  orchitis.  The 
lymphatic  glands  in  the  groin  are  also  enlarged.  After  the 
orchitis  becomes  well  advanced,  the  guinea-pig  may  be  chloro- 
formed and  examined.  Pure  cultures  of  the  specific  organism 
can  be  obtained  in  most  cases  from  the  suppurating  foci  in 
the  testicle.  The  spleen  is  usually  enlarged  and  sprinkled 
with  grayish  nodules.      Other  organs  may  be  involved. 

(2)  Mallein.  Mallein  is  prepared  in  the  same  way  as  tuber- 
culin. It  consists  of  the  glycerinated  bouillon  in  which  the 
glanders  bacteria  have  grown  and  in  which  are  the  products 
resulting  from  their  multiplication.  It  has  a  somewhat  foetid 
odor.  In  applying  the  mallein  test  the  horse  is  injected  usually 
in  the  neck  with  the  required  amount  (0.5  to  2  cc.)  of  mallein, 
the  quantity  depending  upon  the  extent  of  concentration.  If  a 
concentrated  mallein  is  used  it  should  be  diluted  with  a  i  per 
cent  carbolic  acid  solution  to  at  least  2  cc.  The  reaction  is  as 
follows.  In  a  few  hours  there  forms  at  the  place  of  injection 
a  hot,  inflammatory  swelling.  It  i.s  very  painful  and  incase 
of  glanders  quite  large.  From  all  sides  of  the  swelling  there 
may  radiate  wavy  lines  consisting  of  swollen  lymphatics,  hot 
and  painful  when  touched,  extending  toward  the  adjoining 
glands.  When  the  mallein  injection  is  made  aseptically,  this 
swelling  never  suppurates,  but  it  increases  in  size  during  a 
period  of  from  24  to  36  hours  and  persists  for  several  days 
when  it  gradually  diminishes  and  finally  disappears  at  the  end 
of  eight  or  ten  days.  With  the  appearance  of  the  local  swell- 
ing the  patient  becomes  dull  and  dejected,  the  eyes  have  an 
anxious  expression,  the  coat  islusterless,  the  flanks  contracted, 
the  respiration  hurried,  the  appetite  is  impaired,  frequent 
shudders  are  observed  to  pass  through  the  muscles  of  the  fore 
legs  and  sometimes  the  trunk  is  subject  to  violent  convulsive 


124  GLANDERS 

movements.  The  most  active  and  fractions  horses  become 
listless  and  indifferent  to  their  surroundings.  These  general 
phenomena  constitute  what  the  French  call  the  organic  reac- 
tion, but  the\-  are  not  always  so  clearly  marked.  Differences 
in  their  intensity  are  observed  but  they  are  never  completely 
absent. 

The  temperature  reaction  never  fails  to  show  itself.  In 
about  eight  hours  after  the  injection  the  temperature  of  a  glan- 
dered  horse  gradually  rises  1.5",  2°  or  2.5°  F.,  and  even  more 
above  the  normal.  The  rise  in  temperatiire  usualh'  attains  its 
maximum  between  the  tenth  and  twelfth  hour,  occasionally 
not  till  the  fifteenth,  and  more  rareh*  not  until  about  the 
eighteenth  hour.  An  important  fact  to  note  is  that  the  reac- 
tion called  forth  in  glandered  horses  by  the  injection  of  mallein 
persists  for  from  24  to  48  hours  and  in  some  cases  the  temper- 
ature remains  above  the  normal  for  even  a  longer  time.  In 
practice  it  is  advisable  to  take  the  temperature  of  the  suspected 
animals  two  or  three  times  before  the  injection  of  the  mallein, 
and  every  two  hours  beginning  at  the  eighth  and  going  to  the 
twentieth  hour  after  the  injection.  It  is  often  sufficient  for 
diagnostic  purposes  to  take  the  temperature  but  four  times*, 
viz.,  at  9,  12,  15,  and  18  hours  after  the  injection. 

In  health}'  horses  the  injection  of  mallein,  even  in  a  much 
larger  do.se,  produces  no  effect  on  the  temperature  or  the  gen- 
eral condition  of  the  animal.  There  is  produced,  however,  at 
the  point  of  injection,  a  small  oedematous  swelling,  somewhat 
hot  and  painful  to  the  touch,  but  the  oedema  instead  of  in- 
creasing, diminishes  rapidly  and  disappears  in  less  than  24 
hours. 

The  reaction  called  forth  by  the  injection  of  mallein,  in  a 
glandered  animal  is  quite  specific.  When  it  occurs  one  is  en- 
abled to  state  at  once  and  with  certainty  that  glanders  exist, 
although  the  lesions  may  be  quite  minute  or  obscure.  When 
the  reaction  does  not  take  place  it  is  generally  considered  that 
the  animal  tested  is  not  glandered,  although  the  physical 
examination  may  suggest  it.  Notwithstanding  the  specific 
action  of  mallein,  its  administration  can  give  really  useful  indi- 
cations according  to  Nocard   "only  when,  and  as  far  as,  we 


MALLEIN  125 

can  remove  the  causes  of  error  that  have  been  pointed  out  by 
experience."  For  example  it  would  be  imprudent  to  use  nial- 
lein  in  case  of  animals  already  suffering  with  an  abnormal 
temperature.  The  further  precautions  should  be  taken  that 
the  animals  subjected  to  the  test  are  removed  as  far  as  possi- 
ble from  atmospheric  variations  and  the  influence  of  strong 
sun  light,  fog,  rain  and  air  currents.  If  it  be  true  that 
majority  of  horses  are  not  susceptible  or  nearly  so,  to  these 
influences,  there  are  still  some  that  are  afTected  by  them.  So 
that  a  rise  of  1.5  or  2  degrees  in  temperature  would  not  neces- 
sarily indicate  a  reaction.  Again,  it  must  not  be  forgotten 
that  certain  diseases,  strangles  for  instance,  produce  frequently 
great  daily  variations  in  the  temperature,  therefore,  when 
there  is  reason  to  believe  in  the  presence  of  a  disease  of  this 
kind,  it  is  necessary  to  make  sure  that  the  increase  of  tempera- 
ture consequent  on  injection  of  mallein  is  persistent,  and  that 
the  organic  reaction  is  clearl}'  present. 

The  question  ari.ses  whether  animals  found  by  the  help  of 
mallein  to  be  glandered  ought  to  be  immediately  slaughtered  ? 
Xocard  says  no.  The  experience  of  the  last  few  years  goes  to 
prove  that  among  the  animals  that  react  there  are  some  which, 
when  removed  from  the  infected  center  and  thereby  withdrawn 
from  all  chance  of  new  contamination,  recover.  "We  ought 
therefore, ' '  he  continues, '  'to  confine  ourselves  to  the  destruction 
of  those  which  in  addition  to  the  reaction,  present  some  clinical 
indication  of  the  disease,  such  as  ulceration  of  the  nose,  indu- 
rated glands,  suppurative  lymphangitis,  sarcocele  or  other  pro- 
nounced manifestation  of  the  disease.  The  animals  not  showing 
physical  signs  of  affection  must  simply  be  removed  from  among 
the  healthy  horses  and  subjected  from  time  to  time,  say  every 
two  months,  to  the  mallein  test.  If  any  of  these  should 
eventually  show  the  clinical  signs  of  glanders  they  ought  to  be 
slaughtered  at  once.  On  the  other  hand,  those  animals  which 
have  stood  two  successive  doses  of  mallein  without  reacting 
ought  to  be  considered  definitely  cured,  restored  to  their  places 
and  put  to  the  free  disposal  of  the  owners." 

The  views  of  Nocard  are  not  universally  entertained  in  this 
country.    It  has  been  shown  repeatedly  that  a  good  reaction,  fol- 


126  GLANDERS 

lowing  the  injection  of  mallein,  was  a  sure  indication  of  gland- 
ers as  revealed  by  post-mortem.  The  question,  however,  con- 
cerning the  necessity  of  immediate  slaughter  for  purposes  of 
protection,  when  there  are  no  evidences  of  lesions  on  ph3'sical 
examination,  seems  to  be  an  open  one.  This  question  which 
pertains  to  sanitary  police  rests,  until  the  results  of  conclusive 
investigations  are  recorded,  with  those  entrusted  with  the  pro- 
tection of  animals  and  men  from  this  disease.  However,  the 
results  of  certain  experiments  in  the  use  of  mallein  as  a  thera- 
peutic agent,  and  the  fact  that  certain  animals  recover  when 
kept  in  quarantine  are  very  suggestive.  Certainly  further  in- 
vestigations are  needed  to  determine  the  safe  and  equitable  dis- 
position of  animals  devoid  of  all  symptoms  and  obvious  lesions 
of  glanders,  but  which  give  a  reaction  to  the  mallein  test. 

REFERENCES. 

1.  Babes.  Observations  sur  la  morve.  Atch.  de  Med.  Exper.  et 
d'Anai.  Pathologie.     T.  III.     (^1891 )  p.  619. 

2.  Butler.  Glanders.  Bulletin  No.  16.  Miss.  Agr.  Expi.  Sta- 
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3.  Gary.  Glanders.  Bulletin  No.  jj.  Ala.  Agr.  Expt.  Station  0/ 
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4.  DE  SCHWEINITZ  AND  K11.BORNE.  The  use  of  mallein  for  the 
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5.  Francis.  Glanders,  tests  with  mallein.  Bulletin  Ao.  jo. 
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6.  Frothingham.  The  diagnosis  of  glanders  by  the  Strauss 
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10.  Reynolds.  State  control  of  glanders  in  Minnesota.  The 
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Jour,  of  Comparative  Pathology  and  Therapeutics.    Vol.  XI.  ( 1S9S).    p   i. 

12.  Smith.  On  the  influence  of  slight  modifications  of  culture 
media  on  the  growth  of  bacteria  as  illustrated  by  the  glanders  bacillus. 
fournal  of  Comparative  Medicine.     (1890).     p.  158. 

13.  Str.auss.  Sur  un  moyen  diagnostique  rapide  de  la  morve. 
Arch.  de.  Med.  Exper.  ct  d'  Anal.  Path.     T.  III.     (1889)      p.  460. 

14.  Williams.  Glanders.  Bulletin  No.  4.  Montana  Agric. 
Expt.  Station.     1894. 


INFECTIOUS    DISEASES  1 27 

TUBERCULOSIS. 

Synonyms.  Consumption  ;  pearl  disease  ;  phthisis  ;  scro- 
fula (pigs). 

§  105.  Characterization.  Tuberculosis  is  an  infectious 
disease  from  which  the  human  species,  cattle  and  swine  suffer 
very  extensively  and  which,  under  favorable  conditions,  at- 
tacks nearly  if  not  all  species  of  animals  including  fish.  It  is  a 
disease  of  slow  development,  involving  either  primarily,  or  in 
association  with  other  organs,  the  lymphatic  system.  It  is 
characterized  by  the  formation  of  nodules,  or  tubercles,  in 
consequence  of  the  activities  of  the  specific  Baderiuvi  tiibercu- 
losis.  It  does  not  destroy  life  by  acute  toxaemia,  but  by  a 
chronic  and  long  continued  systemic  poisoning  and  by  the 
morbid  changes  brought  about  through  the  localization  of 
these  lesions  in  organs  necessary  to  life. 

§  106.  History.  Tuberculosis  is  one  of  the  oldest  dis- 
eases affecting  cattle  of  which  there  are  identifying  records. 
It  seems  to  have  been  known  to  the  Jewish  people  during  their 
Egyptian  captivity  and  the  ecclesiastical  laws  for  many  cen- 
turies contained  numerous  enactments  against  the  consump- 
tion of  flesh  from  tuberculous  animals.  In  1370,  it  was  for- 
bidden in  Munich  to  have  on  sale  the  flesh  of  animals  affected 
with  tuberculosis.  A  number  of  other  cities  passed  similar 
ordinances.  In  1702,  Florinus  described  the  disease  and 
emphasized  the  then  existing  opinion  that  it  was  identical 
with  syphilis.  This  led  to  the  practice  of  destroying  all  tuber- 
culous animals.  In  1783,  the  Berlin  Board  of  Health  rejected 
the  theory  of  the  connection  of  tuberculosis  and  syphilis  and 
declared  the  flesh  of  affected  animals  to  be  fit  for  food.  This 
led  finally  to  the  cancelling  of  all  laws  throughout  Prussia 
against  the  use  of  flesh  for  food  from  animals  affected  with  the 
disease.  Tscheulin,  in  1816,  recognized  in  reference  to  the 
infection  of  meat,  three  degrees  of  bovine  tuberculosis,  viz  : 
(i)  in  which  the  tubercles  were  to  be  removed  ;  (2)  in  which 
the  diseased  parts  were  to  be  destroyed  and  the  meat  sold  at  a 
low  price  ;  and  (3)  those  cases  in  which  the  lesions  were  so 
extensive  that  the  whole  carcass  must  be  rejected. 


128  TUBERCULOSIS 

The  study  of  the  lesions  themselves  gave  rise  to  a  number 
of  beliefs  concerning  their  nature.  Thus  Virchow,  Schiippel 
and  others  declared  that  the  tubercles  in  cattle  were  lympho- 
sarcomata.  Leisering  considered  them  simply  as  sarcomata. 
Spinola  and  Haubner  maintained  that  human  and  bovine 
tuberculosis  were  identical. 

In  1865,  Villemin  showed  that  tuberculosis  was  due  to  a 
specific  infection.  He  produced  the  disease  in  rabbits  by  in- 
oculating them  with  tuberculous  material  from  human  sub- 
jects. He  also  produced  the  disease  by  feeding  experimental 
animals  and  by  causing  them  to  inhale  tuberculous  material. 
Chauveau,  in  the  same  year,  produced  the  disease  in  cows. 
These  results  were  soon  confirmed  by  Klebs,  Cohnheim  and 
Gerlach.  These  experiments  in  which  the  disease  was  pro- 
duced in  one  species  with  tuberculous  material  from  another 
followed  b}'  the  discovery  by  Koch  of  the  specific  bacterium  of 
the  disease,  led  to  the  view  that  tuberculosis  in  all  species  of 
mammals  was  identical.  This  generall}^  accepted  belief  caused 
sanitarians  to  look  upon  tuberculosis  in  cattle  as  a  great 
menace  to  public  health  with  the  result  that  during  the  closing 
decade  of  the  last  centur3^  this  disease  in  cattle  was  treated 
more  vigorously  as  a  menace  to  the  human  species  than  as  a 
destructive  disease  of  animals. 

In  1896,  Dr.  Theobald  Smith  pointed  out  the  fact  that  for 
certain  animals  the  tubercle  bacteria  from  cattle  were  more 
virulent  than  those  from  man  and  further,  that  there  were  cer- 
tain morphological  and  cultural  differences  existing  between 
them.  In  1898,  he  published  the  results  of  a  more  extended 
series  of  investigations.  Since  that  time  a  number  of  investi- 
gators have  arrived  at  the  same  conclusion.  The  fact  has 
come  to  be  well  known  that  certain  differences  exist  between 
the  bacteria  of  tuberculosis  found  in  the  human  and  in  the 
bovine  species.  Koch's  experiments  reported  at  the  tubercu- 
losis congress  in  London  in  Juh^  1901,  give  additional  evi- 
dence of  a  difference  in  virulence  for  experimental  animals  of 
the  bacteria  of  human  and  of  bovine  tuberculosis.  To  what 
extent  the  human  species  becomes  infected  from  the  bovine 
kind  cannot  be  stated,  but  the  accumulating  evidence  tends  to 


HISTORY  129 

the  conclusion  that  bovine  tuberculosis  is  of  less  significance 
in  its  influence  upon  public  health  than  has  heretofore  been 
thought,  and  of  more  importance  as  a  rapidly  spreading  and 
destructive  disease  among  cattle.  It  is  not  proven,  however, 
that  the  human  species  is  not  affected  with  the  bacteria  of 
bovine  tuberculosis.  The  circumstantial  and  direct  evidence 
is  very  conclusive  that  it  is,  but  that  such  infections  are  not  so 
numerous  as  previously  supposed.  Concerning  its  transmis- 
sion, the  conclusion  seems  to  be  warranted,  that  the  virus  of 
tuberculosis  spreads  very  largeh'  among  men  and  cattle  from 
individual  to  individual  of  the  same  species  rather  than  from 
species  to  species. 

>?  107.  Extent  of  tuberculosis,  especially  among  cat- 
tle and  swine.  The  committee  on  cattle  diseases  and  animal 
food  of  the  American  Public  Health  Association  for  1901 
reported  the  appended  statistics  concerning  the  extent  and  in- 
crease of  tuberculosis  in  cattle  and  swine  in  various  countries. 

"The  slaughter  house  statistics  of  Prussia  show  14.6  per 
cent  of  the  cattle  and  2.14  per  cent  of  the  swine  to  be  tubercu- 
lous. In  Saxony  the  percentage  is  29.13  with  cattle  and  3.10 
with  swine.  In  the  city  of  Leipzig  the  figures  are  36.4  for 
cattle  and  2.17  for  swine.  (Siedamgrotzky).  Of  20,850  ani- 
mals in  Belgium  tested  with  tuberculin  in  1896,  48.88  per  cent 
reacted.  Of  25,439  tested  in  Denmark  from  1893  to  1895, 
49.3  per  cent  reacted  ;  and  of  67,263  tested  from  1896  to  1898, 
32.8  per  cent  reacted  (Bang).  An  examination  of  20,930  cat- 
tle in  Great  Britain,  either  slaughtered  and  examined  post- 
mortem or  tested  with  tuberculin,  showed  5,441  or  26  per  cent 
affected  with  tuberculosis.  M'Fadyean  estimates  that  30  per 
cent  of  the  cows  in  Great  Britain  are  tuberculous.  Figures 
available  in  the  United  States  do  not  cover  a  sufficient  area  of 
our  territory  to  allow  us  to  make  a  reliable  estimate  of  the  ex- 
tent of  tuberculosis  in  milch  cows." 

"Our  beef  cattle  as  they  come  to  the  large  packing  houses, 
are  yet  comparatively  free  from  tuberculosis.  Of  4,841, 166  cattle 
slaughtered  in  the  year  1900,  under  Federal  meat  inspection, 
but  5,279  or  o.ii  per  cent  were  sufficiently  affected  to  cause 
the  condemnation  of  any  part  of  the  carcass.     Of  23,336,884 


130  TUBERCULOSIS 


hogs  similarly  inspected,  5,440  were  sufficiently  affected  to 
cause  a  condemnation  of  some  part  of  the  carcass.  This  is 
equal  to  0.023  per  cent,  or  slightly  more  than  one-fifth  the 
proportion  found  in  beef  cattle." 

"  The  slaughter  house  statistics  of  all  countries  show  that 
the  percentage  of  affected  hogs  increases  as  the  disease  be- 
comes more  common  in  cattle,  so  that  we  must  consider  not 
only  the  effect  of  the  disease  upon  beef  and  milk  producing 
animals,  but  also  upon  swine.  Tuberculosis  is  more  acute 
with  hogs  than  with  cattle,  and  there  is  a  much  greater  ten- 
dency to  generalization,  consequently  the  parts  used  for 
human  food  are  more  likely  to  be  affected,  and  if  there  is  a 
possibility  to  communicate  the  virus  through  the  meat  the 
danger  is  increased  by  this  peculiarity  of  the  disease  in  swine." 

§  108.  Geographical  distribution.  Tuberculosis  is  an 
exceedingly  wide  spread  disease.  In  earlier  times  it  was  quite 
prevalent  among  cattle  in  central  Europe.  It  seems  to  have 
existed  in  Western  Asia  and  Northern  Africa  at  an  early  date. 
From  these  centers  it  has  spread  to  nearly  every  cattle  raising 
country  of  the  world.  Its  rapid  spread  during  the  last  fifty 
years  is  attributed  to  the  increase  in  cattle  exchange  resulting 
in  the  introduction  of  tuberculous  animals  into  healthy  herds. 
It  is  stated  that  in  many  countries,  and  in  large  districts  with- 
in others,  tuberculosis  did  not  exist  until  it  was  introduced 
within  recent  years  by  the  importation  of  diseased    animals. 

In  countries  where  there  has  been  little  or  no  importation 
of  cattle,  and  in  which  the  native  breeds  still  exist  unchanged, 
as  in  many  parts  of  Russia,  Austria  and  Spain,  in  the  north- 
ern part  of  Sweden  and  Norway,  and  in  parts  of  Africa, 
tuberculosis  is  practically  unknown.  This  is  true  of  the  cattle 
on  the  island  of  Jersey  where  for  more  than  a  hundred  years 
foreign  cattle  have  not  been  introduced. 

In  the  United  States  the  disease  is  very  widely  distributed. 
It  is  found  to  a  considerable  extent  in  certain  localities  where 
the  climatic  conditions  seem  to  be  beneficial  for  tuberculous 
people.  The  explanation  for  this  seems  to  be  that  tuberculous 
animals  have  been  introduced  into  certain  herds  in  these  dis- 
tricts.    There  are,  however,  large  areas  in  which  it  is  practi- 


ETIOLOGY  I  3  r 

cally  unknown.  The  Western  steers  that  are  killed  in  the 
slaughter  houses  of  Kansas  City,  Omaha,  Sioux  City  and 
Chicago  are  practically  free  from  this  disease.  In  many  locali- 
ties, especially  where  there  is  an  extensive  interchange  of 
animals,  a  large  percentage  of  the  herds  are  more  or  less 
affected. 

§  log.     Etiology.  Tuberculosis  is  caused  ,  ^ 

by  a  rodshaped  organism  known  as  Bader-  /  '  ^  i  y 
ium  tuberculosis.  It  was  discovered  by  Rob- 
ert Koch  in  1882.  Schiiller  and  Toussaint 
had  previously  studied  growths  which  seem, 
from  the  results  of  their  inoculation  experi- 
ments, to  have  been  this  organism.  The  bac- 
terium of  tuberculosis  is  a  slender  rod-shaped  Fig  23.  Bac- 
organism  with  rounded  ends,  from  2  to  5//  in  terimn  of  iuher- 
length  and  from  o  3  to  o-5//  broad.  The  rods  c'^^^sis. 
are  straight  or  slightly  curved,  and  occur  singly,  in  pairs  or 
in  small  bundles.  Frequently  they  cross  one  another.  They 
do  not  produce  spores,  but  vacuoles  are  often  observed  and 
branching  forms  have  been  described. 

The  bacterium  of  tuberculosis  is  readih-  cultivated  on  arti- 
ficial media  such  as  blood  serum,  glycerinated  agar  and  bouil- 
lon, and  potato  after  it  has  been  adapted  to  such  artificial  con- 
ditions.*    It  is,  however,  not  easy  to  cultivate  it  directly  from 


*To  accomplish  this  necessitates  a  very  special  and  careful  proce- 
dure. Dr.  Theobald  Smith,  of  Harvard  University  (Jour,  of  Exp.  Med., 
Vol.  HI.,  1898,  p.  45r),  has  the  credit  of  formulating  a  method  by  com- 
bining details  in  such  a  manner  that  the  procuring  of  cultures  is,  in 
•most  cases,  possible.  Dog  serum  is  used.  The  method,  as  he  gives  it,  is 
as  follows,  viz.  : — 

"The  dog  was  bled  under  chloroform  and  the  blood  drawn  from  a 
femoral  artery,  under  aseptic  conditions,  through  sterile  tubes  directly 
into  sterile  flasks.  The  serum  was  drawn  from  the  clots  with  sterile 
pipettes  and  either  distributed  at  once  into  tubes  or  else  stored  with  0.25 
to  o  3  per  cent  chloroform  added.  Discontinued  sterilization  was  ren- 
dered unnecessary.  The  temperature  required  to  produce  a  sufficiently 
firm  and  yet  not  too  hard  and  dry  serum  is  for  the  dog  75°  to  76°  C.  For 
horse  serum  it  is  from  4°  to  5°  lower.  The  serum  was  set  in  a  thermo- 
stat into  which  a  large  dish  of  water  was  always  placed  to  forestall  any 
abstraction  of  moisture   from   the  serum.     About  3  hours  suffice  for  the 


132  TUBERCULOSIS 

ordinary  tuberculous  lesions.  Although  in  the  beginning,  the 
tubercle  bacteria  from  man  and  from  animals  were  believed  to 
be  entirely  identical,  they  have  been  found  to  possess  slightly 
different  characters  and  properties.  Smith  pointed  out  in 
1898,  that  morphologically  those  from  cattle  were  shorter  and 
thicker  than  those  from  man,  that  they  grew  slightly  different 
on  blood  serum,  and  that  they  were  much  more  virulent  for 
cattle  and  rabbits  than  those  from  the  human  species.  Since 
that  time  his  conclusions  have  been  confirmed  by  a  number  of 
investigators.  Koch  has  recently  obtained  like  results.  At 
present,  therefore,  we  must  look  upon  the  tubercle  bacteria 
coming  from  these  different  species  as  possessing  races  or 
varieties  which,  perhaps,  are  the  results  of  their  different  con- 
ditions of  life.  The  investigations  which  have  been  made 
with  the  decidedly  different  forms  of  this  organism  found  in 
in  tuberculosis  of  fowls  and  of  fish  have  led  a  few  experimen- 
ters to  believe  that  they  are  simply  varieties  of  the  organism 
first  described  b}-  Koch.  Further  inquiries  are  necessary  to 
fully  satisfy  bacteriologists  that  all  of  these  forms  are  thus  re- 
lated to  the  one  species.  There  seems  to  be  no  reason  for 
doubting  that  the  bovine  and  human  forms  are  varieties  or 
races  of  the  same  species.  The  difference  in  the  conditions  of 
life  under  which  they  exist  in  the  bodies  of  men  and  of  cattle 
are  quite  enough  to  explain  resulting  differences  in  the 
bacteria. 


coagulation.  When  serum  containing  chloroform  is  to  be  coagulated,  I 
am  in  the  habit  of  placing  the  tubes  for  an  hour  or  longer  in  a  water 
bath  at  55°  to  60"^  C,  or  under  the  receiver  of  an  air  pump,  to  drive 
off  the  antiseptic.  This  procedure  dispenses  with  all  sterilization  ex- 
cepting that  going  on  during  the  coagulation  of  the  serum.  It  prevents 
the  gradual  formation  of  membranes  of  salts,  which,  remaining  on  the 
surface  during  coagulation,  form  a  film  unsuited  for  bacteria.  Tubes  of 
coagulated  serum  should  be  kept  in  a  cold  closed  space  where  the  oppor- 
tunities for  evaporation  are  slight.  They  should  always  be  kept 
inclined. 

"The  ordinary  cotton-plugged  test  tubes  I  do  not  use,  because  of 
the  rapid  dr\'ing  out  permitted  by  them,  as  well  as  the  opportunities  for 
infection  with  fungi.  Instead,  a  tube  is  used  which  has  a  ground  glass 
cap  fitted  over  it.  This  cap  contracts  into  a  narrow  tube  plugged  with 
glass  wool.     This  plug  is  not  disturbed.     The  tube  is  cleaned,  filled,  and 


SYMPTOMS  1 33 

no.  Symptoms.  The  symptoms  vary  according  to  the 
course  of  the  disease.  Two  classes  are  recognized,  viz. -.(i)  the 
chronic  form,  which  is  most  common,  and  (2)  the  acute  form 
or  mihary  tuberculosis. 

The  symptoms  of  chronic  tuberculosis  depend  upon  the 
location  of  the  lesions  and  their  extent.  When  the  lesions  are 
situated  deeply  and  are  not  of  great  extent,  they  may  exhibit 
no  visible  evidence  of  their  presence.  In  such  cases  the  in- 
fected animal  may  present  the  picture  of  perfect  health  and 
show  no  disturbance  of  function.   Indeed,  some  animals  in  which 


inoculated  by  removing  the  cap.  With  sufficient  opportunity  for  the  in- 
terchange of  air  little  evaporation  takes  place,  and  contamination  of  the 
culture  is  of  very  rare  occurrence.  In  inoculating  these  tubes,  bits  of 
tissue,  which  include  tuberculous  foci,  especially  the  most  recent,  are 
torn  from  the  organs  and  transferred  to  the  serum.  Very  little  crushing, 
if  any,  is  desirable  or  necessary.  I  think  many  failures  are  due  to  the 
often  futile  attempts  to  break  up  firm  tubercules.  Nor  should  the  bits  of 
tissue  be  rubbed  into  the  surface,  as  is  sometimes  recommended.  After 
a  stay  of  several  weeks  in  the  therniostat,  I  usually  remove  the  tubes 
and  stir  about  the  bits  of  tissue.  This  frequently  is  the  occasion  for  a 
prompt  appearance  of  growth  within  a  week,  as  it  seems  to  put  certain 
still  microscopic  colonies  in  or  around  the  tissue  into  better  condition 
for  further  development.  The  thermostat  should  be  fairly  constant,  as 
urged  by  Koch  in  his  classic  monograph,  but  I  look  upon  moisture 
as  more  important.  If  possible,  a  thermostat  should  be  used  which  is 
opened  only  occasionally  Into  this  a  large  dish  of  water  is  placed, 
which  keeps  the  space  saturated.  Ventilation  should  be  restricted  to  a 
minimum.  As  a  consequence,  moulds  grow  luxuriantly  and  even  the 
gummed  labels  must  be  replaced  by  pieces  of  stiff  nianila  paper  fastened 
to  the  tube  with  a  rubber  band.  By  keeping  the  tubes  inclined,  no 
undue  amount  of  condensation  water  can  collect  in  the  bottom,  and  the 
upper  portion  of  the  serum  remains  moist.  The  only  precaution  to  be 
applied  to  prevent  infection  with  moulds  is  to  thoroughly  flame  the 
joint  between  tube  and  cap  as  well  as  the  plugged  end,  before  opening 
the  tube.  When  test  tubes  are  employed  it  is  well  to  dip  the  lower  end 
of  the  plug  into  sterile  molten  paraffin  and  to  cover  the  tube  with  a 
sterilized  paper  cap.  The  white  bottle  caps  of  the  druggist  are  very  ser- 
viceable." 

While  the  tuberculous  material  is  perfectly  fresh  (uncontaminated ) 
and  in  the  early  stages  of  the  disease,  it  is  safer  to  inoculate  a  guinea 
pig,  and  after  the  lesions  begin  to  develop  to  chloroform  it  and  make 
the  cultures  from  the  recently  a-ffected  liver  or  spleen. 


134  TUBERCULOSIS 

the  lesions  are  both  extensive  and  widel}-  distributed  and  which 
have  never  presented  noticeable  signs  of  the  disease,  are  killed 
in  prime  condition  for  beef  without  a  suspicion  of  the  presence 
of  disease. 

Since  the  lesions  of  tuberculosis  vary  so  much  in  different 
cases,  it  is  not  possible  to  give  a  description  of  what  can  be 
designated  the  characteristic  or  even  the  usual  sj'mptoms  of 
this  disease.  There  are,  however,  certain  general  manifestions 
that  appear  in  most  of  the  advanced  cases,  such  as  emaciation, 
while  the  appetite  continues  good.  This  is  always  a  suspicious 
indication  and  especially  if  accompanied  by  cough,  rough  coat 
and  tight,  harsh  skin.  Rough  or  loud  respiratory  sounds  are 
suspicious,  and,  in  advanced  cases,  it  is  often  found  that  the 
animal  groans  when  pressure  is  brought  to  bear  upon  the  chest 
wall.  Many  cases  bloat  habitually,  and  hard,  painless  swell- 
ings (enlarged  lymphatic  glands)  beneath  the  skin  in  the  region 
of  the  escutcheon,  flank,  shoulder  or  throat  are  suspicious. 

In  tuberculosis  of  the  lungs,  it  may  be  said  that  coughing 
is  the  most  noticeable  symptom.  It  is  most  common  after 
feeding,  drinking,  or  after  rapid  moving  following  a  period  of 
repose,  but  sometimes  it  occurs  without  any  apparent  cause. 
The  cough  is  usualh'  strong,  dry  and  frequently  of  a  high 
pitch.  Sometimes  it  is  very  violent  accompanied  by  protru- 
sion of  the  tongue.  Auscultation  reveals  modified  and  abnor- 
mal .sounds  of  different  kinds  in  the  lungs  ;  sibilant,  sonorous 
and  mucous  rales  are  most  common.  A  dull  sound  is  often 
detected  on  percussion.  It  is  also  to  be  noted  that  this  condi- 
tion is  of  slow  development  and  long  duration,  thus  aiding  one 
to  distinguish  it,  in  many  cases,  from  bronchitis  or  pneumonia. 

Where  the  mediastinal  lymphatic  glands  are  enlarged  and 
press  upon  the  oesophagus,  it  is  stated  that  the  animal  bloats 
habitually.  Chronic  or  habitual  bloating  accompanied  by  a 
good  appetite  and  no  other  evidence  of  disease  of  the  digestive 
tract,  especially  if  there  is  shortness  of  breath  and  cough, 
may  be  looked  upon  as  strongh'  indicative  of  tuberculosis  with 
enlarged  mediastinal  lymphatic  glands. 

Sometimes  large  tubercular  masses  develop  on  the  pleura. 
In  such  cases  the  principal  symptom  is  a  friction  sound  that  is 


SYMPTOMS  135 

heard  most  distinctly  during  inspiration.  If  the  masses  are  large 
enough  they  give  rise  to  a  dull  sound  upon  percussion.  In 
tuberculosis  of  the  stomach  and  intestines,  digestion  is  in- 
terfered with.  This  gives  rise  to  poor  appetite,  frequently 
to  diarrhoea  and  sometimes  to  alternation  of  diarrhoea  and 
constipation.  In  tuberculosis  of  the  peritoneum  or  of  the  lining 
of  the  abdominal  cavity,  the  lymphatic  glands  of  the  flank  are 
often  enlarged  and  hard.  Sometimes  this  condition  can  be 
diagnosed  positiveh' by  a  rectal  examination  and  the  discovery 
by  this  means  of  the  hard,  nodular  masses.  Tuberculosis  of 
the  liver  does  not  give  rise  to  obvious  symptoms  unless  the 
disease  is  far  advanced,  in  which  case  jaundice  may  be  observed. 

In  animals  in  which  the  post-pharyngeal  lymphatic  glands 
are  enlarged  from  tuberculosis,  the  breathing  is  harsh  and 
noisy.  In  this  condition  there  is  sometimes  difficulty  in  swal- 
lowing, and  particles  of  chewed  up  food  are  occasionally  expelled 
from  the  mouth,  either  voluntarily,  when  it  is  found  that  they 
cannot  be  swallowed  conveniently,  or  by  the  coughing  they 
occasion  upon  reaching  the  pharynx.  These  enlarged  glands 
may  sometimes  be  detected  by  palpation  accomplished  by  plac- 
ing one  hand  on  each  side  of  the  throat  above  the  larynx  and 
then  pressing  from  opposite  sides. 

Tuberculosis  of  the  udder  is  detected  by  an  enlargement 
and  hardening  of  the  affected  part,  usually  by  the  absence  of 
pain  and  the  fact  that  the  secretion  is  not  altered  until  the  part 
has  been  diseased  for  some  time.  In  advanced  cases,  instead 
of  milk,  the  udder  secretes  a  yellowish,  cloudy  and  sometimes 
flocculent  fluid.  In  acute,  rapidly  developing  cases,  there  may 
be  pain  and  oedema  of  the  skin.  In  nearly  all  cases  of  udder 
tuberculosis  the  supra-mammary  lymphatic  glands,  situated 
above  the  udder  in  the  middle  of  the  escutcheon  are  enlarged 
and  hard.  If  there  is  doubt  as  to  the  character  of  the  di.sease 
of  the  udder,  the  milk,  or  possibly  a  piece  of  excised  udder 
tissue,  may  be  examined  bacteriologically. 

In  tuberculosis  of  the  brain,  the  animal  is  unsteady  and 
uncertain  in  its  movements.  It  lies  down  much  of  the  time,  is 
usually  subject  to  occasional  cramps  and  is  apt  to  carry  the 
head  in   an   unusual  position.     Such  cases  are  inclined  to  in- 


136  TUBERCULOSIS 

crease  rapidly  and  terminate  in  death  following  coma  or  con- 
vulsions. In  tubercular  disease  of  the  bones  and  joints,  the 
parts  are  enlarged,  there  is  loss  of  motion,  pain  and  usually 
abscess  formation  followed  by  the  discharge  of  thick  yellow 
pus.  In  tuberculosis  of  the  uterus  or  ovaries  and  sometimes 
in  peritoneal  tuberculosis  in  the  cow,  the  subject  is  almost 
continually  in  heat.  In  tuberculosis  of  the  uterus,  there  is 
sometimes  a  discharge  of  thick,  yellowish  material  mixed  with 
mucus  and  slime.  In  tuberculosis  of  the  testicles  the  organs 
become  enlarged  and  hard. 

In  all  advanced  cases  the  nutrition  of  the  animal  is  inter- 
fered with  and,  sooner. or  later,  the  "tuberculous  cachexia" 
appears.  It  is,  however,  in  many  cases  remarkable  to  note  the 
extent  of  lesions  in  animals  that  are  well  nourished  and  pres- 
ent no  external  signs  of  disease.  Animals  killed  in  prime 
condition  by  the  butcher  are  sometimes  found  to  contain  ex- 
tensive and  widely  distributed  lesions  of  tuberculosis.  In 
general  tuberculosis,  many  of  the  symptoms  described  above 
may  occur  simultaneously.  The  symptoms  of  acute  miliary 
tuberculosis  "  galloping  consumption  "  are  rapid  loss  of  flesh, 
depression,  poor  appetite,  cough,  weakness,  rapid  breathing, 
harsh  respirator}-  .sounds,  some  elevation  in  temperature,  in- 
creased pulse  rate  and,  sometimes,  enlarged  lymphatic  glands. 
The  course  of  this  form  of  tuberculosis  is  always  rapid  and 
terminates  in  death.  Acute  miliary  tuberculosis  occurs  when 
large  numbers  of  tubercle  bacilli  are  discharged  into  the  blood 
or  lymph  currents.  They  are  then  carried  to  other  parts  of  the 
body,  filtered  out  in  the  capillaries  of  the  lungs,  liver,  spleen, 
kidneys  and  elsewhere,  causing  tubercular  lesions  in  each  of 
these  localities.  The  lesion  from  which  the  infectious  material 
entered  the  circulation  ma}-  have  been  a  comparatively  small 
nodule.  This  form  of  the  disease  is  more  likely  to  appear  in 
young  animals  than  in  adults,  and  is  more  common  among 
swine  than  in  cattle. 


MORBID    ANATOMY 


■67 


ij  III.  Morbid 
anatomy.  The  usual 
direct  ana  t  o  m  i  c  a  1 
changes  following  the 
invasion  of  tubercle 
bacteria  are  the  forma- 
tion of  nodules  or 
tubercles.  A  tubercle 
has  been  defined  as, 
"a  small  nonvascular 
nodule  compose  d  o  f 
cells  varying  in  form 
and  size  with  some 
basement  substa  nee 
between  the  m  a  n  d 
with  an  inherent  ten- 
dency to  undergo 
central  necrosis. ' '  In 
a  large  numbe  r  o  f 
cases    the    individual  Fig.  24.     Right  lateral  aspect  of  posterior 

tubercles   are  distinct    half  of  steer's  head,     {a)  lower  jaw.    (b)  ear 

.  ..  .        passage.      [c)    horn,     id)   styloid  process  of 

and    easilj'    recogmz-   -^       *  .    ;     ^ 


able  while  in  others 
they  are  coales  c  e  d 
forming  a  mass  of 
necrotic    tissue.     The 


occipital  bone,  (e)  parotid  gland,  (f)  sub- 
maxillary gland.  A.  right  parotid  lymph 
gland.  B.  right  post  maxillary  lymph 
gland.  C.  right  submaxillary  lymph  gland. 
Lvniph  glands  often  the  scat  of  tubercular  de- 

1      •  .^  posits.     (Smith.) 

lesions     vary,     there-   ^  ^ 

fore,  from  well  isolated  minute  or  larger  nodules  to  masses  or 
cavities  containing  a  purulent,  caseous,  or  calcified  substance. 
The  location  of  the  primary  lesion  depends  upon  the  chan- 
nel of  infection.  If  the  specific  organisms  are  lodged  in  the 
oral  cavity  or  pharynx  they  may,  through  an  accidental  abra- 
sion of  the  mucosa,  be  taken  to  some  of  the  lymphatic  glands 
about  the  head  :  if  they  are  taken  directly  through  the  respira- 
tory passages  into  the  lungs  they  either  develop  nodules  in  the 
lung  tissue  proper,  or  they  are  carried  through  the  lymphatic 
system  to  the  lymph  glands  draining  the  lungs  where  the  lesions 
first  appear.      If  the   specific  bacteria  are  first  lodged  in  the 


I. -.8 


TUBERCULOSIS 


intestinal  mucosa, 
primary  tubercular 
ulcers  may  develop 
or  they  may  pass 
into  the  mesenteric 
lymphatics  or  the 
portal  vein.  It  may 
happen  that  the 
bacteria  may  be  car- 
ried by  means  of 
the  lymph  or  blood 
stream  and  lodge  in 
any  part  of  the 
body,  such  as  the 
brain,  kidneys, 
spleen,  testes,  ovar- 
ies, bones,  joints, 
and  subcutaneous 
and  intermuscular 
glands  and  serous 
membranes.       The 

Fig.  25.  Dorsal  aspect  of  bovine  lungs.  a-a\^^'^^^^'^^  ^t  hand, 
highland  /eft  caudal  lobes.  b-b\  r.  and  I.  ven-  however,  seems  to 
tral  lobes.  c-c\  first  and  second  right  cephalic  show  that  in  a  laro-e 
-lobes.  C-,  left  cephalic  lobe,  c,  trachea,  x  x,  ^ajoritv  of  cases 
region  most  frequently  involved  in  the  earliest    ,  .  '  .      . 

stages  of  pulmonary  tuberculosis.     The   lesious  P^'i^ary  lesions 

nre  usually  at  this  stage  embedded  in  the  lung  are  (i)  in  the  lungs 
tissue.    (Smith.)  or     the     lymphatic 

glands  draining  them,  (2)  in  the  lymphatic  glands  about  the 
head,  (3)  the  intestines  and  mesenteric  glands,  and  (4)  in  the 
portal  glands  or  liver  substance  itself.  Primary  lesions  some- 
times occur  in  the  generative  organs  and  udder. 

It  not  infrequently  happens  that  the  apparent  primary 
lesions  occur  on  the  pleura,  peritoneum,  meninges  or  synovial 
membranes  while  the  organs  remain  free  from  disease.  In  such 
cases  the  lesions  consist  of  many  tubercles  varying  from 
one  to  ten  or  more  millimeters  in  diameter  or  of  bunches  of 
closely  set  tubercles  which  are  more  or  less  flattened  or  irregular 


MORBID    ANATOMY 


139 


in  shape  owing  to  their 
mutual  pressure  (Fig. 
31).  Sometimes  these 
tubercles  are  attached  to 
the  serous  membrane  by 
a  small,  tough,  fibrous 
pedicle  ;  frequently, how- 
ever, this  is  absent  and 
the  nodules  rest  bodily 
upon  the  membrane. 

The  structure  of  the 
tubercle  consists,  in  the 
beginning,  of  a  few  cells 
surrounding  the  invad- 
ing specific  organisms. 
These  are  soon  encased 
by  a  zone  of  epithelioid 
cells  and  giant  cells 
which  is  soon  sur- 
rounded by  an  outer 
layer  of  round  or  lym- 
phoid cells.  The  central 
portion  becomes  necrosed 
and  as  the  nodule  en- 
larges the  central  ne- 
crotic portion  becomes 
correspondingly  large.  In 
cattle  there  is  a  strong 
tendency  for  the  necrotic 
tissue  to  become  infil- 
trated with  lime  salts 
and    encapsulated    (Fig. 


Fig.  26.  Trachea  and  bronchial 
tubes  of  bovine  lungs  showing  at- 
tached bronchial  glands.  a. a.,  supply 
right  afid  left  caudal  lobes,  b.b.,  supply 
r.  and  I.  ventral  lobes.  c-c\  branches  of 
its  right  supernumerary  bronchus.  C-,  sup- 
ply left  cephalic  lobe,  d,  branch  to  azygos 
lobe,  e,  trachea.  A,  left  bronchial  lymph 
gland.  B,  right  bronchial  lymph  gland. 
C,  lymph  gland  base  of  supn .  bronchus.  D, 
gland  often  between  bronchi.    The  glands 


A.  to  D.are  often  involved.  (Smith.) 
32).  In  certain  other  species  a  deposit  of  fibrous  tissue  in 
the  outer  zone  of  the  tubercle  has  been  observed.  In  the 
smaller  and  more  susceptible  experimental  animals  such  as  the 
guinea  pig  and  rabbit  and  frequently  in  swine,  the  lesions  are 
of  a  more  diffuse  nature  infiltrating  the  interstitial  tissue  with 
the  tuberculous  mass  and  gradually  encroaching  upon  the  par- 
enchyma.    Circumscribed  tubercles  may  also  be  present. 


140 


TUBERCULOSIS 


generalized 


In  secondary  or 
tuber- 
culosis one  or  more 
of  the  organs, 
omentum,  serous 
membranes, or  lym- 
phatic system  may 
become  more  or  less 
thickly  sprinkled 
with  minute  grey- 
ish nodules  about 
the  size  of  a  millet 
seed.  These  tuber- 
cles are  at  first  al- 
most the  color  of 
mother-of-pearl  but 
later  as  the  central 
caseous  degenera- 
tion begins  they  be- 
c  o  m  e    grayish. 


Giant  cells  are  usu- 
ally numerous. 

In  studying  the 
lesions  in  a  fatal 
case  of  tuberculosis 


Fig.  27.  Dorsal  aspect  of  bovine  lutigs  show, 
ing  position  of  the  posterior  mediastinal  glands, 
a,  d,  c,  c'.,  caudal,  ventral,  cephalic  lobes,  f 
oesophagus,  g.  muscular  pillars  of  diaphragm- 
h.  posterior  aorta.  ^.  left  bronchial  gland, 
i.  caudal  margin  of  the  ligatnefit  of  the  lung 
Mediastinal  glands  are  shown,  most  of  them 
resting  on  the  oesophagus.  The  large  caudal 
one  may  find  with  gland  restiyig  on  the  pillars  of  the  diaphragm  is 
varjuno"  mod  ifica-  most  frequently  diseased  and  often  attains  an 
tions  one  or  more  of  enormous  size.  The  remaining  mediastinal 
,,      P  ,,        .  ,.      glands  are  arranged  in  two  sets  on  the  right  and 

thetollowmgcondi-    ,  .,  ■       ^,,  ^,  ,c     n  X 

°  left  margins  oj  the  oesophagus.     {^mUh.) 

tions,  viz. 

( 1 )  The  primary  lesion  may  be  found  in  any  one  of  the 
organs  or  membranes.  Its  comparative  age  is  determined  by 
the  character  of  the  anatomical  changes.  It  may  be  entirelj- 
encysted,  caseous  or  calcareous  and  dead.  In  addition  to  this 
primar}^  focus,  there  may  be  a  succession  of  tubercles  of  various 
ages  distributed  in  one  or  more  organs. 

(2)  The  lesions  may  be  restricted  to  one  organ,  as  the 
liver  in  which  the  primary  focus  has  spread  by  continuity  due 


Plate  II. 


TUBERCULOUS  HEART  FROM  A  COW. 


V  of 


v>^^^^f: 


CAUVf^ 


MORBID    ANATOMY 


141 


to  its  infiltrating  nature  until  the  destruction  of  the  tissues  of 
the  organ  has  become  so  extensive  that  death  results.  Such 
cases  do  not  seem  to  be  common. 

(3)  The  primary  lesion  may  be  well  marked  and  accom- 
panied by  miliary  tubercles  sprinkled  extensively  throughout 
the  organs    and  tissues  of  the  entire  body. 

(4)  The  lesions  throughout  the  body  may  resemble  each 
other  very  closely  so  that  difficulty  may  be  experienced  in 
determining  the  primary  focus. 

In  the  lungs,  two  distinct 
forms  of  lesions  are  observed. 
(i)  The  air  cells  maybe  infil- 
trated with  the  tuberculous  mass 
spreading  directly  from  the  pri- 
mary focus.  This  may  be  puru- 
lent, caseous  or  calcareous.  The 
color  may  be  whitish,  gray  or  of 
a  yellowish  tinge.  (2)  The  le- 
sions may  consist  of  miliary 
tubercles.  In  later  stages  these 
nodules,  more  or  less  translucent, 
may  become  yellowish,  caseated 
and  calcareous  in  their  centers. 
Large  tubercular  nodules  are 
frequently  formed  by  the  massing 
of  several  of  these  minute  tuber- 
cles. 

When  the  lungs  are  pri- 
marily attacked  the  caudal 
(principal)  lobes  are  most  fre- 
quently involved.  Smith  con- 
siders the  seeming  predilection 
for  the  larger  lobes  to  be  due  to 
mechanical     conditions.       The 

writer  has  found,  however,    that  puration.  (a)  caseous 

cous  centers. 


Fig.    28.      Tuberculous  focus 
'ith  center,   {c)   undergoing  sup- 


(b)  calcar- 

in  certain  herds  that  have  been 

killed   after   the   tuberculin   test,  the   primary  and   only   lung 

lesions  were  in  the  ventral  and  cephalic  lobes.      It  is  important 


Fig.  29.     Photograph  of  a  porlion  of  tubercular  omentum  of  a  cow, 
showing  the  tubercles,  natural  size. 


]MORBID    ANATOMY 


H3 


to  note  that  usually  the  bronchial  glands  are  also  involved. 
When  the  pleurae  are  affected  the  lesions  consist  of  nodules 
varying  in  size  from  that  of  a  millet  seed  to  a  large  pea, 
sprinkled  more  or  less  thickly  on  one  or  both  of  the  visceral  or 
parietal  surfaces.  These  form  the  "pearl  disease"  {Perlsiicht) 
of  the  German  and  the  "grape  disease"  of  the  English  writers. 
If  they  become  confluent,  large  masses  are  found. 


Fig.  30.     Photograph  of  pleura  shelving  suiall  tubercular  tiodules. 

Tuberculosis  of  the  thoracic  glands  is  ver}'  common  and 
usually  accompanies  lesions  in  the  lungs  ;  but  often  the  lungs 
may  be  healthy  and  the  glands  involved.  (See  figures  for 
location  of  glandsj.  The  primary  lesions  maybe  and  often 
are  found  in  the  lymphatic  glands  about  the  head. 

In  the  abdominal  cavity  the  organs  most  frequenth'  in- 
volved are  the  peritoneum,  mesenteric  lymph  glands,  portal 
lymph  glands  and  liver.  The  kidneys,  spleen,  ovaries  and  uterus 
are  more  rarely  the  seat  of  tuberculous  tumors.  Ulcers  in  the 
intestine  have  not  been  common  in  the  writer's  observation. 
Tuberculosis  of   the   testis   is   sometimes    found.     The  udder 


144  TUBERCULOSIS 

often  becomes  the   seat  of  tubercular   deposits  in  cases  of  gen- 
eralized tuberculosis. 

When  the  primary  infection  is  restricted  to  a  single  focus 
the  disease  is  said  to  be  localized.  When  the  specific  bac- 
teria are  spread  from  the  primary  lesion  through  the  agency 
of  the  lymph  and  blood  streams,  sprinkling  other  organs  with 
the  infecting  bacteria  each  of  which  becomes  the  starting  point 
for  the'development  of  a  new  tubercle,  the  disease  has  become 
generalized.* 

It  was  formerly  considered  that  when  the  lesions  existed 
in  both  of  the  large  (abdominal  and  thoracic)  cavities  of  the 
body  the  disease  was  generalized.  It  is  possible,  however,  for 
it  to  be  generalized  when  the  lesions  are  restricted  to  the 
oro-ans  of  one  cavitv  as  the  secondarv  seeding  with  the  bacteria 
that  have  escaped  from  a  primary  focus  through  the  circulation 
may  be  restricted  to  the  cavity  in  which  the  first  lesion  devel- 
oped. It  seems  better,  therefore,  to  accept  Ostertag's  views  and 
classify  local  and  general  tuberculosis  in  accordance  with  the 
nature  of  the  lesions  rather  than  their  distribution  in  the  body. 

The  fact  is  worthy  of  consideration,  that  very  often  cattle 
killed  after  reacting  to  tuberculin  do  not  show  extensive  dis- 
tribution of  lesions.  Frequently  animals  are  killed  soon  after 
infection  has  taken  place,  in  which  ca.se  the  lesions  are  re- 
stricted to  a  single  lymphatic  gland  or  other  organ.  In  other 
cases  old  lesions  of  considerable  proportion  are  found  as  shown 
in  plate  11,  where  the  heart  muscle  was  entirely  enca.sed  in  a 
thick  calcareous  tubercular  deposit.  In  this  case,  the  animal 
was  in  good  flesh  and  killed  for  beef  without  a  suspicion  that 
it  was  in  any  way  diseased. 

i^  112.  Tuberculosis  in  swine.  Channels  of  infection. 
It  is  stated  that  young  animals  belonging  to  the  precocious 
breeds  seem  to  be  more  liable  to  tuberculosis  than  others.  In 
nine  cases  out  of  ten  the  animals  are  infected  by  ingestion.  The 
pig  easily  becomes  tuberculous  when  fed  on  material  rich  in 
tubercle  bacteria.  If  pigs  are  fed  on  the  refuse  from  dairies 
and    cheese   manufactories   in   districts   where  there  is  much 

*The  Federal  meat  inspection  regulations  state,  that  animals  affected 
with  "extensive  or  generalized  tuberculosis"  are  to  be  condemned. 


TUBERCULOSIS    IX    SWIxXE 


145 


tuberculosis  in  cattle  or  on  tuberculous  viscera  they  readily  be- 
come infected.  Infection  through  the  respiratory  tract,  while 
it  is  certainly  possible,  seems  to  be  rare.  The  piggeries  where 
the  refuse  from  butter  and  cheese  factories  is  fed  and  those 
which  adjoin  abattoirs  supply  the  majority  of  animals  found 
on  post-mortem  to  be  tuberculous. 


®-^®oo5»®£? 


■3  ~'X'@,<;\? 0  0  -Tw-ic 


-* «,:-.®  ~^^.  9  ©  i.'a  v>^ » ®  ^i>  ^.-i.-^j  :..  O^^A  Al  ® . 


of iOJl*^/».  ^ 


Fig.  31.     A  drawing  of  a  section  of  a   very  young  tubercle  in  spleen. 
{  Thoma). 

Ostertag  has  called  special  attention  to  this  disease  as 
existing  among  swine  in  certain  parts  of  northern  Denmark 
and  Germany,  where  there  was  much  tuberculosis  in  cattle, 
and  where  swine  were  fed  upon  the  slime  from  creamery  sepa- 
rators. Experiments  show  the  possibility  of  infection  by 
means  of  the  sputum  of  tuberculous  people. 

In  the  cases  which  have  come  to  our  notice  there  is  very 
strong  evidence  that  the  swine  were  infected  by  being  fed  upon 
milk  from  tuberculous  cows.  In  one  of  these  cases,  the  tuber- 
culin test  showed  that  a  large  number  of  the  cows  from  which 
the  milk  was  obtained  were  affected. 


Fig.  32.  Photograph  of  a  section  from  anterior  lobe  of  a  tuberculous 
lung  of  a  cow,  showing  rounded  tubercular  infiltration  and  calcified 
centers.     {Lazu.) 


TUBERCULOSIS    IN    SWIXE  I  47 

§  113.  Symptoms.  In  most  cases  tuberculosis  of  the 
pig  is  first  recognized  at  the  abattoir.  Sometimes,  however,  it 
causes  local  and  general  troubles,  which  vary  according  to  the 
organ  or  system  attacked.  The  following  symptoms  have 
been  noted. 

Its  localization  in  the  abdominal  organs  causes  the  arrest 
of  fattening  and  the  progressive  wasting  of  the  subject.  The 
mucous  membranes  become  pale  ;  the  hide  becomes  dirty  ; 
there  is  usually  either  constipation  or  diarrhoea.  The  animal 
is  in  low  spirits  and  remains  buried  in  its  straw  for  entire 
days  ;  the  corkscrew  of  its  tail  is  straightened  ;  the  abdomen 
is  pendulous  and  the  eyes  sunken  ;  palpation  of  the  abdomen  is 
painful  and  may  reveal  more  or  less  voluminous  masses,  due  to 
the  changes  in  the  mesenteric  glands.  It  is  common  to  find 
glandular  tumors  in  the  submaxillary  region  at  the  level  of  or  at 
the  thoracic  inlet.  In  this  form  the  malady  may  last  several 
months,  but  death  supervenes  rapidly  if  the  lesions  are  general- 
ized through  the  blood  stream.  Primary  pulmonary  tuberculosis 
is  very  rare  but  sooner  or  later  lung  lesions  complicate  abdominal 
tuberculosis,  and  betray  themselves  at  the  outset  by  a  short,  dry, 
abortive  cough  and  by  difficult  respiration.  The  cough  soon 
becomes  paroxysmal  and  painful  and  is  often  followed  by 
vomiting  ;  the  respiration  becomes  hurried  and  gradually  pain- 
ful and  more  difficult  :  wasting  is  very  rapid  and  death  super- 
venes in  a  few  weeks. 

The  scrofula  of  swine  (glandular  tuberculosis)  usually 
shows  it.self  by  a  puffing  up  of  the  face,  which  a  careful  exam- 
ination shows  to  be  lifted  up  by  the  subjacent  glands,  which 
are  enlarged,  indurated,  still  fairly  mobile  and  free  from  heat 
or  tenderness.  The  retro-pharyngeal,  superior  cervical,  and 
sublingual  glands  usually  take  part  in  the  lesion,  forming  a  kind 
of  necklace  of  unequal  and  knotty  tumors,  which  extend  from 
-ear  to  ear,  and  become  larger  under  the  neck  between  the  two 
of  the  lower  jaw.  Similar  tumors  may  be  developed  at  the  rami, 
thoracic  inlet,  behind  the  shoulder  or  in  the  groin,  which,  as 
they  increase  in  size,  become  harder  and  more  adherent  to  the 
neighboring  tissues.  Sometimes,  however,  a  slight  fluctuation 
is  perceptible  ;  the  tumor    softens,  then  forms  an  abscess  and 


148  TUBERCULOSIS    IN   SWINE 

discharges  a  small  quantity  of  thick  and  grumous  pus  ;  but  the 
glandular  tumor  does  not  disappear  and  the  opening  into  the 
abscess  remains  for  a  long  time  as  a  fistula. 

At  the  same  time  one  may  notice  swellings  of  the  bones, 
causing  a  true  tuberculous  arthritis  when  the  lesions  happen 
to  be  situated  at  the  level  of  an  epiphysis.  Persistent  lame- 
ness, fistulous  wounds  suppurating  indefinitely,  necrosis, 
caries,  etc.,  are  the  compHcations  of  the  lesions  of  the  bone, 
the  development  of  which  is  always  extremely  slow. 

§  114.  Morbid  anatomy.  The  manifestations  of  tuber- 
culosis in  swine,  as  suggested  in  the  foregoing  statement,  are 
exceedingly  interesting.  Nocard  finds  the  lesions  to  consist 
of  miliary  granulations  which  rapidly  become  caseous,  as  in 
cattle,  but  which  more  rarely  contain  calcareous  salts.  Gene- 
ralization is  common,  in  which  case  the  viscera  are  thickly 
sprinkled  with  gray  granulations  which  are  translucent 
throughout,  or  opaque  in  their  centers,  and  quite  analogous  to 
those  found  in  tubercular  lesions  in  other  animals. 

As  the  disease  most  often  results  from  ingestion  of  the 
virus,  the  digestive  apparatus  and  the  corresponding  lymphatic 
glands  (submaxillary,  parotid,  pharyngeal,  superior  cervical, 
mesenteric,  sublumbar,  etc.  )  may  be  decidedly  altered,  while 
the  other  organs  remain  practically  intact.  Lesions  of  the 
small  intestine  and  the  caecum  are  common  and  take  the  form 
of  ulcers  of  the  mucous  membrane,  of  miliary  nodules  or  of 
tuberculous  infiltrations  involving  at  once  the  mucous,  the 
muscular,  and  subserous  tissues.  The  lesions  in  the  liver  take 
the  form  either  of  miliary  granulations,  which  are  yellow  and 
caseous  and  scattered  in  great  numbers  through  the  thickness 
of  the  organ,  or  else  of  rounded  nodules  which  are  yellowish 
white  in  color,  varying  in  size  from  that  of  a  pea  to  a  hazel 
nut,  and  of  a  tough  consistency.  On  section  they  appear  some- 
times to  be  firm,  homogeneous  and  fibrous  ;  sometimes  soft- 
ened in  the  center,  but  rarely  infiltrated  with  calcareous  salts. 
The  peritoneum  and  the  pleura  are  sometimes  the  seat  of  an 
eruption  of  fine  granulations  which  remain  in  a  state  of  miliary 
nodules.  Lesions  like  those  in  the  liver  may  exist  in  the  lungs, 
but  generally  there  is   found  in   these   organs  an  innumerable 


Plate  III. 


TUBERCULOUS    SPLEEN    OF    HOG. 


SPLEEN    OF    HEALTHY    HOG. 


MORBID    ANATOMY  1 49 

quantity  of  minute  translucent,  gray  granulations,  caused  by 
generalization  through  the  blood  stream,  in  which  case  the 
liver,  the  spleen,  the  kidneys,  the  medulla  of  the  bones,  and 
the  manmiae  are  usually  infiltrated  with  similar  growths. 

It  is  common  to  find  lesions  localized  in  one  or  several 
lymphatic  glands.  The  tonsils  and  the  pharyngeal  or  sub- 
maxillary glands  are  the  ones  most  often  affected.  They  be- 
come voluminous,  hard  and  knotty,  as  they  have  undergone 
a  true  fibrous  transformation  and,  consequentl\%  difficult  to  cut. 
This  is  shown  by  the  tissues  creaking  under  the  cutting  in- 
strument. In  section  they  have  the  appearance  of  old  fibrous 
tissue  ;  here  and  there  small  yellow  foci  are  seen  of  a  softer 
consistency,  almost  caseous  ;  sometimes  veritable  purulent  col- 
lections are  found,  either  encysted  or  in  communication  with 
the  exterior.  If  one  submits  the  caseous  or  purulent  matter  to 
a  bacteriological  examination,  tubercle  bacteria  are  not  usually 
found.  The  bacterium,  however,  is  present  and  if  this  matter 
is  inoculated  into  the  peritoneal  cavity  or  the  cellular  tissue  of 
guinea  pigs  it  will  produce  tuberculosis. 

These  chronic  glandular  lesions,  with  their  very  slow  pro- 
gress, have  long  been  looked  upon  as  constituting  the  scrofula 
of  swine,  and  to  scrofula  was  also  assigned  the  tuberculous 
lesions  of  bones  (ribs,  vertebrae,  articulations,  shoulder  blades, 
hip  bones,  etc.)  which  are  common  in  pigs,  both  young  and  old. 

The  older  authors  noted  that  the  ancient  scrofula  was  often 
accompanied  by  visceral  tuberculosis,  but  they  refused  to  admit 
the  identity  and  even  the  relationship  of  the  two  affections. 

The  generalization  of  the  di.sease  especially  in  the  mus- 
cular tissue  is  reported  by  several  observers.  Moule  calls  at- 
tention to  this  peculiarity  of  the  disease.  Stockman  shows 
that  while  the  disease  is  ordinarily  generalized,  muscular  le- 
sions may  exist  in  swine  in  the  absence  of  generalization. 
Zschokke  has  called  special  attention  to  the  localization  of 
tubercular  lesions  in  the  head  of  swine,  especially  in  the  nares 
and  brain. 

Tuberculosis  in  the  horse  is  rare  although  a  total  of  many 
cases  has  been  reported.  Bang  has  collected  twenty-nine  cases. 
In  Saxony  .08  per  cent  of  the  horses  (3,500)  that  were  slaugh- 


150  TUBERCULOSIS 

tered  were  tuberculous.  In  this  and  most  countries  there  are 
no  reliable  statistics  respecting  the  extent  of  the  disease  in 
this  species.  M'Fadyean  has  pointed  out  the  fact  that  in  a 
considerable  number  of  cases  of  equine  tuberculosis,  where  the 
horses  have  been  fed  milk  from  tuberculous  cows,  the  morbid 
anatomy  differs  but  slightly  from  that  in  tuberculous  cattle. 

Sheep  and  other  domestic  animals  are  reported  to  suffer 
more  or  less  extensively  from  this  disease.  All  of  the  so-called 
tuberculosis  in  sheep  and  fowls  which  I  have  been  able  to  ex- 
amine proved  not  to  be  tuberculosis  but  animal  parasitisms 
such  as  the  "nodular  disease  of  sheep"  and  "taeniasis"  in 
fowls. 

^^  115.  Differential  diagnosis.  Tuberculosis  is  to  be 
differentiated  from  actinomycosis,  glanders,  and  various  parasit- 
isms resulting  in  nodules  largely  in  the  walls  of  the  intestine. 
In  cattle  the  nodules  are  produced  by  an  Oesophagostoma,  in 
sheep  the  nodules  are  caused  by  Oesophagostoma  Columbianum 
Curtice.  In  chickens  a  nodular  taeniasis  of  the  intestine  is  not 
infrequently  mistaken  for  tuberculosis.  Abscesses  and  necrotic 
foci  due  to  various  agencies  must  also  be  distinguished  from 
tubercular  lesions. 

In  cases  of  actinomycosis,  the  ray  fungus  can  usually  be 
detected  on  a  microscopic  examination.  Bad.  mallei  can  be 
found  either  in  cultures  or  by  guinea  pig  inoculations  in  cases  of 
glanders,  and  in  parasitic  diseases  the  specific  animal  parasite 
can  be  found  if  diligently  sought.  A  careful  study  of  the 
recent  lesions,  especially  in  the  nodules  caused  by  the  animal 
parasites  will  show  that  they  are  not  structurally  like  the 
tubercle  as  described  above. 

From  the  symptoms  and  morbid  anatomy  it  is  clear  that 
hard  and  fast  lines  for  diagnosing  tuberculosis  cannot  be  laid 
down.  As  a  rule,  the  lesions  are  characteristic  although  there  are 
many  exceptions.  In  making  a  positive  diagnosis,  one  must  rely 
upon  the  discovery,  microscopically,  of  the  specific  bacterium, 
the  result  of  animal  inoculation  or  the  effect  of  tuberculin. 

The  tubercle  bacteria  can  be  found  by  making  and  properly 
staining  cover-glass  preparations  from  the  tuberculous  tissues 
or  discharges  in  a  certain  number  of  cases.      When  these  tuber- 


Plate   IV. 


TUBERCULOUS    LUNGS    OF    HOC 


From   tSiil    .Vti   jH. 


DIFFERENTIAI,   DIAGNOSIS  151 

cular  lesions  open  into  the  respiratory  tract  the  specific  bac- 
teria can  ahnost  always  be  found  in  the  expectoration.  This 
is  especially  true  in  men  and  Ravenel  has  shown  that  it  is  often 
true  in  cattle.  In  old  and  in  the  very  recent  tuberculous 
lesions,  it  is  not  so  easy  to  detect  these  organisms  microscopic- 
ally. When  there  is  doubt  the  animal  inoculation  gives  quite 
prompt  results. 

§  116.  Animal  inoculation  for  purposes  of  diagnosis. 
Guinea  pigs  are  preferable,  although  rabbits  may  be  used. 
With  tuberculous  tissue  either  of  two  methods  may  be  em- 
ployed, (i)  A  small  piece  (about  the  size  of  a  pea  or  bean)  of 
the  tissue  may  be  inserted  under  the  skin  by  first  making  an 
incision  with  a  .sharp  scalpel  through  the  skin  and  superficial 
fascia,  and  then  with  a  pair  of  fine  forceps  insert  the  bit  of 
tissue  well  under  the  skin  and  close  the  opening  with  one  or 
more  sutures.  (2)  The  tissue  may  be  crushed  in  a  mortar  and 
thoroughly  mixed  with  a  few  cubic  centimeters  of  sterile  w^ater 
or  bouillon  and  then  injected  with  a  hypodermic  syringe.  The 
needle  should  be  of  large  calibre.  If  it  is  suspected  milk  it 
may  be  injected  into  the  abdominal  cavity.  If  the  material  is 
tuberculous  and  contains  living  tubercle  bacteria,  the  death  of 
the  animal  follows  in  from  three  weeks  to  four  months.  Usually 
the  lymphatic  glands  in  the  groin  and  axilla  are  enlarged  and 
often  caseous.  If  a  guinea  pig  is  u.scd,  the  liver,  spleen,  lungs 
and  kidneys  are  liable  to  be  affected,  in  the  order  named  ;  if  a 
rabbit,  the  lungs  are  often  the  first  of  the  viscera  to  be 
attacked. 

§  117.  Tuberculin  test.  The  tuberculin  test  is  the  best 
practically  and  in  a  large  majority  of  tuberculous  cases  among 
animals  and  in  man  the  only  means  of  positively  detecting  the 
di.sease  in  the  living  individual. 

Tuberculin.  Tuberculin  is  the  concentrated  liquid,  usually 
glycerinated  bouillon,  on  which  tubercle  bacteria  have  grown 
until  the  products  resulting  from  their  multiplication  have 
become  imparted  to  the  medium  in  sufficient  quantity  to  inhibit 
their  further  development.  It  is  not  definitely  determined  just 
what  these  products  are  or  just  how  they  are  elaborated. 
Briefly  stated,  the  preparation  of  tuberculin  consists  in  the 
following  procedures,  viz  : 


152  TUBERCULOSIS 

(i)  The  preparation  of  the  culture  medium  (glycerin- 
ated  bouillon),  distributing  it  in  suitable  flasks  and  inoculating 
it  with  the  growth  from  a  pure  culture  of  tubercle  bacteria. 

(2)  The  flasks  are  placed  in  an  incubator  at  a  tempera- 
ture of  about  37°  C.  where  they  remain  until  the  growth 
ceases.  The  length  of  time  necessary  to  accomplish  this 
depends  upon  the  age  and  condition  of  the  culture  from  which 
the  inoculations  were  made.  From  four  to  ten  weeks  are 
usually  required. 

(3)  After  the  maximum  growth  is  attained,  the  cultures 
are  sterilized  by  heat,  either  by  boiling  in  a  closed  water  bath 
or  heating  to  a  higher  temperature  in  an  autoclav. 

( 4)  After  sterilization,  the  cultures  are  filtered  to  remove 
all  of  the  dead  bacteria,  and  then  the  filtrate  is  evaporated  over 
a  water  bath  to  the  desired  degree. 

(5)  The  concentrated  liquid  is  passed  through  a  Pasteur 
or  Berkefelter  filter,  standardized,  bottled  and  labeled  for  dis- 
tribution. It  should  be  perfectly  clear  although  its  color  may 
vary.      If  it  is  cloudy  it  should  be  rejected. 

It  will  be  seen  from  the  method  of  preparation  that  tuber- 
culin cannot  possibly  contain  living  tubercle  bacteria.  It  is 
heated  on  two  occasions  to  a  temperature  and  for  a  length  of 
time  far  in  excess  of  that  required  to  destroy  them  besides 
being  passed  through  a  filter  capable  of  removing  all  bacteria. 

The  original  tuberculin  or  lymph  of  Koch  was  concen- 
trated to  one-tenth  of  the  volume  of  the  saturated  culture. 
This  gave  a  thick,  syrupy  liquid  owing  to  the  presence  of  the 
glycerine.  The  diagnostic  dose  which  came  to  be  recom- 
mended for  cattle  of  medium  weight  was  0.25  c.c.  On  account 
of  its  consistency  as  well  as  the  minuteness  of  the  dose,  it  was 
found  to  be  practicable  to  dilute  this  quantity  with  seven  parts  of 
a  diluent.  A  weak  solution  of  carbolic  acid  was  ordinarily  used. 
The  difficulties  and  the  danger  of  contamination  involved  in 
making  the  dilutions  in  the  field  led  to  the  method  of  diluting 
the  tuberculin  in  the  laboratory  before  sending  it  out.  This 
has  been  the  practice  of  the  Bureau  of  Animal  Industry  for  a 
number  of  years.  Equally  as  good  results  are  obtained  b}' 
concentrating  the  saturated  culture  to  the  point  where  2C.c. 


TUBERCULIN  1 53. 

contains  an  equivalent  of  the  0.25  c.c.  of  the  highly  concen- 
trated lymph.  This  process  avoids  the  necessity  of  dilutions 
and,  with  the  addition  of  a  few  drops  of  carbolic  acid,  the 
weaker  solution  keeps  perfectly. 

Tuberculin  in  the  dose  necessary  to  bring  out  its  diagnostic 
effect  is  absolutelj^  harmless  to  a  healthy  animal.  Thousands- 
of  observations  which  have  been  reported  assure  us  of  this  fact. 
Tuberculin  is  in  dail}-  use  in  every  state  in  the  Union,  in  Can- 
ada and  in  every  country  in  Europe,  yet  so  far  as  can  be 
learned  not  a  single  case  of  injury  following  its  use  in  healths- 
cattle  has  been  reported.  In  the  tuberculous  animal  it  pro- 
duces a  rise  of  temperature  which,  within  certain  limits,  follows 
a  definite  course  usually  terminating  in  from  18  to  24  hours 
after  the  injection.  The  temperature  usually  begins  to  rise  in 
about  eight  hours  giving  a  stead\-  but  quite  rapid  elevation  for 
from  I  to  3  hours.  A  continuous  high  elevation  for  from  2  to  4 
hours,  possibly  longer,  and  a  gradual  decline.  This  is  prac- 
tically constant,  be  the  raise  moderate  or  extreme.  In  addi- 
tion to  the  elevation  in  temperature  there  is  sometimes  a 
marked  nervous  chill.  Why  we  get  this  reaction-'^  is  not 
positively  determined. 


*Trudeau  (Johns  Hopkins  Hospital  Bulletin,  July,  1899)  gives  the  fol- 
lowing summary  of  the  mechanism  of  the  tuberculin  reaction.  "The  most 
generally  accepted  theory  at  present  in  regard  to  it  is,  briefly,  the  small 
dose  of  tuberculin  injected  is  a  partly  specific  irritant  both  to  tuberculous- 
foci  and  to  the  susceptible  organism  in  general.  It  produces  intense  hyper- 
aemia  of  all  tuberculous  tissue  in  the  body  (local  reaction),  and  as  the  re- 
sult of  this  hyperaemia  nmch  toxin  stored  up  in  the  tubercles  themselves 
is  thrown  into  the  general  circulation  and  produces  fever  and  character- 
istic symptoms  which  go  to  make  up  what  is  termed  'a  general  reaction.' 
That  these  poisons  stirred  up  in  the  tubercles  are  in  part  at  least  derived 
from  the  dead  or  weakened  bacilli  has  been  shown  by  the  experiments- 
of  Babes  and  Proca,  who  found  that  if  two  sets  of  rabbits  be  injected 
with  equal  quantities  of  living  and  dead  bacilli,  the  latter  react  to  the 
tuberculin  test  at  a  much  earlier  period  than  those  inoculated  with  liv- 
ing germs.  This  hypothesis  that  the  general  reaction  is  brought  about 
by  toxins  already  stored  up  in  the  tuberculous  lesions  and  exploded  as 
it  were  by  the  hyperaemia  produced  about  these  lesions  as  the  result  of 
the  test  injection  of  tuberculin,  is  borne  out  by  the  fact  that  a  greater 
amount  of  albumose  can  be  recovered  from  the  evaporated  urine  col- 


154  TUBERCULOSIvS 

Applying  the  hiberculhi  test.  In  brief,  the  method  for  ap- 
plying the  tuberculin  test  in  cattle  is  as  follows  : 

1.  The  normal  temperature  of  the  animal  to  be  tested 
must  be  determined.  It  is  recommended  that  it  be  taken 
hourly  or  ever}'  two  hours  for  the  day  preceding  the  test. 

2.  The  tuberculin  is  injected  subcutaneously  in  the  side 
of  the  neck.  Care  must  be  taken  that  the  syringe  is  sterile 
and  the  site  of  injection  should  be  disinfected.  The  size  of 
the  dose  depends  upon  the  preparation  of  tuberculin. 

3.  Beginning  6  or  8  hours  after  the  injection,  the  tem- 
perature should  be  taken  hourly  or  at  least  every  two  hours 
for  fully  three-fourths  of  a  day. 

4.  During  the  time  of  testing,  the  cattle  should  be  kept 
quiet,  free  from  all  exposure,  and  fed  normally. 

5.  In  case  of  reaction,  there  should  be  a  rise  of  at  least 
1.5°  F.  above  the  maximum  individual  normal  temperature  as 
determined  on  the  preceding  day.  The  elevation  should  come 
on  gradually,  remaining  practically  at  its  fastigium  for  a  few 
hours  and  gradually  subside.  Erratic  elevations  of  short  dura- 
tion are  to  be  excluded.  In  cases  of  doubt  the  animals  should 
be  retested. 

6.  Animals  advanced  in  pregnancy  and  tho.se  known  to 
be  suffering  from  any  disease  or  in  oestrum  should  be  excluded. 
All  methods  of  treatment  including  exposure  to  cold,  kind  of 
food  and  drink  which  would  tend  to  modify  the  temperature 
should  be  avoided.  Animals  in  which  the  disease  is  well 
advanced  sometimes  fail  to  react. 

7.  The  dose  should  vary  to  correspond  with  the  weight 
of  the  animal.  In  cases  of  a  second  test,  within  a  few  days, 
the  quantity  of  tuberculin  injected  should  be  larger  than  for 
the  first  test. 


lected  during  the  reaction  than  was  contained  in  the  test  injection  ; 
also  by  clinical  observations  which  indicate  that  patients  suffering  from 
localized  surgical  tuberculous  processes  of  limited  extent,  and  where  the 
vascular  supply  to  the  part  is  limited,  require  a  larger  test  injection  to 
produce  the  reaction  than  those  who  have  extensive  or  scattered  visceral 
lesions  in  highly  vascular  organs  like  the  lungs."  The  reader  is  referred 
to  this  paper  for  a  careful  consideration  of  the  vexed  questions  relating 
to  tuberculosis. 


TUBERCULIN 


155 


In  cattle  there  is  a  marked 
variation  in  tlie  normal  daily  tem- 
perature. A  fluctuation  of  two  or 
even  three  degrees  within  24  hours 
is  frequently  found.  Cold  water 
when  drunk  in  considerable  quanti- 
ties lowers  the  temperature  from 
two  to  four  degrees.  A  temporary 
excitement  usually  causes  an  eleva- 
tion of  from  I  to  1.5°  F.  There 
are  also  marked  variations  in  the 
temperature  of  the  same  animal  on 
consecutive  days.  The  tempera- 
ture at  12  noon  and  12  midnight 
are  often  the  same.  In  some  cases 
the  maximum  elevation  for  the  day 
occurs  near  midnight  and  on  the 
following  day  the  minimum  tem- 
perature appears  at  that  time.  It 
is  not  uncommon  for  the  maximum 
temperature  to  occur  twice  in  the 
same  day  and  occasionally  several 
times  within  the  twenty-four  hours. 
There  are  marked  individual  varia- 
tions in  the  effect  of  ordinary  con- 
ditions upon  the  temperature  such 
as  food,  excitement  or  tempera- 
ture of  the  air.  A  hot  spell  causes 
a  rise  of  two  and  in  some  ca.ses  four 
degrees.  The  average  temperature 
of  the  animals  in  three  herds  tested 
by  Howe  and  Ryder  were  102.5°, 
102.6°  and  101°  F.  respectively. 

In  a  well  kept  Government 
herd  that  was  tested  with  tubercu- 
lin, the  temperature  of  part  of  the 
animals  was  taken  hourly  for  24 
and  part  of  them  for  16  hours  pre- 
ceding the  injection.     An  examina- 


;x* 


tw 


? 


.--11 


^' 


Av, 


v^  ffAf. 


Fig.  33.  Tuberculous  spleen 
from  a  pig.     {Law.) 


156 


TUBERCULOSIS 


lion  of  the  records-^  shows  the  averag'e  daily  v^ariatioii  of  20  ani- 
mals in  which  the  temperature  was  taken  for  24  hours  to  be 
2.31°  F.  The  maximum  individual  variation  in  a  single  day 
was  4. 3°  F. ,  the  minimum  0.5°  F.  In  25  other  animals  where  the 
temperature  was  taken  for  16  hours,  the  average  variation  was 
1.79°  F.  In  these  the  maximum  variation  was  3.2°  F.,  the 
minimum  0.6°  F.  Ten  healthy  animals  (did  not  react  to 
tuberculin)  in  the  same  herd  gave  an  average  variation  of 
2.08°  F.  In  these  the  maximum  daily  variation  was  4.1°  F., 
the  minimum  1°  F.  The  lowest  temperature  was  usually,  but 
not  invariably,  in  the  morning  and  the  highest  in  the  after- 
noon or  evening.  I  have  appended  the  records  of  the  temper- 
ature of  two  of  these  animals. 


THE   INITIAL   TEMPERATURE   OF   TWO   COWS,  WITH    RATE   OF   PULSE 
AND   NUMBER    OF   RESPIRATIONS   PER    MINUTE. 


Cow,  N 

0.  I 

Cow,  N 

0.  2 

Hour 

Tempera- 
ture 

Pulse 

Resp. 

Tempera- 
ture 

Pulse 

Resp. 

9  A.  M. 

99.8 

48 

18 

98. 6 

48 

15 

10 

99-5 

66 

18 

98.6 

60 

15 

II       " 

99.0 

60 

15 

99.0 

60 

15 

12         " 

1 00. 8 

54 

15 

99-4 

54 

15 

I    p.    M. 

101.4 

54 

15 

1 00.0 

54 

18 

2         " 

ior.6 

48 

15 

100.2 

54 

18 

3      " 

102.0 

60 

24 

100.4 

72 

24 

4      " 

103.0 

66 

24 

102.7 

72 

24 

5      " 

103.3 

66 

24 

102  8 

72 

27 

6      " 

103. 1 

57 

18 

103.0 

60 

27 

7 

102.2 

60 

20 

102.4 

60 

24 

8      " 

103.0 

56 

16 

102.0 

60 

24 

9      " 

103.1 

52 

24 

102.2 

50 

24 

10 

102.5 

60 

20 

102.0 

50 

18 

II      " 

102.5 

60 

20 

102.0 

60 

20 

12  midnight 

102  4 

56 

16 

ior.6 

54 

20 

I    A.   M. 

loi.S 

60 

20 

101.4 

5S 

24 

2       " 

102.0 

64 

18 

102.2 

58 

18 

1       * ' 
J 

102.0 

60 

18 

101.6 

58 

18 

4      " 

102.2 

54 

24 

101.5 

60 

24 

5      " 

101.6 

56 

24 

102.0 

60 

18 

6      " 

101.8 

60 

18 

102.2 

60 

20 

8      " 

102.5 

56 

16 

103.2 

60 

18 

*Bulletin  No.  7,  Bureau  of  Animal  Industrj',  U.  S.  Department  of 
Agriculture,  Washington,  D.  C.  The  tests  were  made  by  Drs.  F.  L. 
Kilborne  and  E.  C.  Schroeder,  under  the  direction  of  Dr.  Theobald  Smith. 


NORMAL   TEMPERATURE 


O/ 


In  view  of  these  normal  temperature  variations,  which 
often  exceed  the  tubercuHn  reaction,  it  is  obvious  that  before 
applying  the  test  the  normal  temperature  of  the  animals  should 
be  approximately  determined  and  that  when  they  are  being  sub- 
jected to  the  test  they  should  be  cautiously  protected,  other- 
wise the  comparatively  slight  elevation  necessary  to  detect  the 
disease  may  be  disguised. 


f-.OO 

s-.io 

S.ZO 

3-.30 

S.^O 

s.so 

6./0 

y.oo 

e.c>- 

'?.S(. 

/^ 

/03 

'OZ 

,^DflA  N 

■ELY 

or   y/A 

reR    A 

T   JS'/ 

lOI 

\ 

1 
1 

lOO 

1 

99 

_^ 

^ 

^ 

I 

Fig.  34.     Chaii  showing  the  effect  of  drinkivg  cold  water  upon  the  tem- 
perature of  a  cow. 

As  the  reaction  seems  to  be  the  result  of  an  affinity  exist- 
ing between  the  tuberculin  and  the  living  tuberculous  lesion, 
it  is  natural  to  suppose  that  when  the  two  are  brought  together 
in  the  same  animal  it  would  invariabh^  take  place.  Experi- 
ence has  shown  that  it  almost  always  does.  It  is  important  to 
understand,  as  far  as  possible,  the  reason  for  the  exceptions 
and  the  extent  to  which  they  occur.  The  reported  failures  of 
the  tuberculin  tests  fall  into  two  distinct  classes  : 

( i)  When  there  is  a  reaction  and  no  disease  is  found.  In 
explaining  this  alleged  error,  the  records  of  the  cases  which 
have  come  to  my  attention  have  been  so  deficient  in  data  con- 
cerning the  normal  temperature  variation  of  the  animals,  and 
the  incompleteness  of  the  post-mortem  examinations,  that  it 
seems  possible  for  the  error  to  rest  with  the  observer  quite  as 
much  as  with  the  tuberculin.  Unfortunately  we  are  as  yet 
unable  to  determine,  by  the  reaction,  the  extent  of  the  disease. 


158 


TUBERCULOSIS 


SO  that  a  beginning  lesion  no  larger  than  a  walnut  may  cause 
a  pronounced  rise  of  temperature  and  such  a  tubercle  may  be 
difficult  to  find,  especially  if  located  in  the  marrow  of  some 
bone. 

(2)  Where  there  is  no  reaction  and  the  disease  exists.  It 
is  generally  admitted  that  advanced  cases  often  fail  to  react, 
but  here  the  test  itself  is  of  little  importance  as  the  disease  can 
be  detected  by  the  clinition  on  physical  examination.  When, 
however,  tuberculin  is  carefully  prepared  and  scientifically 
administered,  these  exceptions  are  exceedingly  rare. 

The  practical  value  of  tubercuhn,  however,  lies  in  its  effi- 
ciency in  the  arts  of  comparative  and  sanitary  medicine.  It  is 
in  the  practical  application  that  difficulties  are  encountered. 
The  many  details  and  precautions  enumerated  as  absolutely 
fiouFfs  ArrER  Injection 


Fig.  35.     Irregular  temperatures  following  tuberculin  that  are  not  caused  by 
tuberculosis.     ( Curtice. ) 

essential  to  the  best  results  are  often  considered  too  tedious  and 
time  consuming,  and  consequently  the  practice  has  come  too 
generally  into  vogue  of  neglecting  or  ignoring  many  of  the 
precautions.  In  order  that  the  te.st  may  be  practicable,  some 
practitioners  resort  to  a  shorter  method  of  procedure  even  at 
the  risk  of  an  occasional  error. 

§  118.  Prevention.  Tuberculosis,  like  other  infectious 
diseases,  can  be  very  largely  prevented.  To  accomplish  this  it 
is  necessary  to  keep  tuberculous  animals  from  entering  the 


PREVENTION 


159 


healthy  herds.  If  they  are  admitted  and  later  the  fact  is  dis- 
covered, it  is  necessary  to  remove  them  and  to  thoroughly 
disinfect  the  stable.  In  eliminating  the  disease  from  a  herd, 
b}'  means  of  the  tuberculin  test,  it  is  necessary  to  retest  the 


4./^. 
9.00 

//OO 

P.M. 
/.oo 

.3.00 

^.00 

y.oo 

900 

//  00 

A.M. 
/OO       J.OO 

^00 

yoct 

s 

/06 

/ 

^~^"-v^ 

S 
/OS 

V 

~~^-~- 

\ 

\, 

5 

\ 

^t 

/Of- 

\, 

s 

/OS 

/ 

\ 

s^ 

/ 

\ 

/ox 

V 

/  \ 

^ 

M/i/<crt 

/6 

// 

~-~~~^ 

^-^ 

s 

/Ol 

\ 

y 

/fr 

,^--^ 

^ 

/ 

y 

s 
/oo 

\ 

A 

// 

s 

39 

'^///rc 

1    /S 

M 

Fig.  36.  Temperature  cui'zie  of  a  tuberculous  cow  for  48  hours.  The  Hue 
A.  A.  shoivs  temperature  for  24  hours  preceding  the  injection  of  tuberculin 
ivhich  ivas  injected  at  q  a.  m. ,  March  16  ;  b.  b.  b.  shows  the  temperature  for  the 
24  hours  after  the  tuberculin  itijectio7i. 

non-reacting  animals  after  six  months  or  a  year  has  passed  in 
order  to  find  any  case  that  might  have  been  infected,  but  in 
which  the  disease  had  not  begun  to  develop,  at  the  time  of  the 
first  test. 

REFERENCES. 

1.  Adami.  On  the  significance  of  bovine  tuberculosis  and  its  erad- 
ication and  prevention  in  Canada.  Canadian  four,  of  Jledicine  and 
Surgery.     Dec.  1899 

2.  Curtice  The  detection  of  tuberculosis  in  cattle.  Annual  Re- 
port, Bureau  of  Animal  Industry,  U.  S.  Dept.  Agric.     1S95-96. 

3.  Koch.  The  etiology  of  tuberculosis.  Mitt,  aus  dem.  Kaiserl. 
Gesundheitsamte.  Vol.  II.  1S84.  Translated  in  Vol.  CXV.  New 
Sydenham  Society-. 

4.  Koch.  The  combating  of  tuberculosis  in  the  light  of  the  exper- 
ience that  has  been  gained  in  the  successful  combating  of  other  infec- 
tious diseases.     Am.  Vet.  Review.     Vol.  XXV.     No.  6^     Sept.     1901. 


l6o  TUBERCULOSIS 

5.  Moore  and  Dawson.  Tuberculosis  in  swine,  the  nature  of 
the  disease  with  a  report  of  three  cases.  Annual  Report,  Bureau  of 
Animal  Industry,  U.  S.  Dept.  Agric.     1895-96. 

6.  Moore.  The  preparation  of  tuberculin,  its  value  as  a  diagnostic 
agent,  and  remarks  on  the  human  and  bovine  tubercle  bacilli.  Trans, 
of  the  Med.  Society  of  the  State  of  N.  V.     1900. 

7.  NoCARD.     The  animal  Tuberculoses.     New  York. 

8.  Pearson.  The  Pennsylvania  plan  fur  controlling  tuberculosis 
of  cattle.     Froc.  Am.  Vet.  Med.  Assn.     1S99. 

9.  Pe.arson.  Tuberculosis  in  cattle  and  the  Penn.  plan  of  its 
repression.     Bulletin  7,-      Penn.  Dept.  of  Agr.     1901. 

10.  Pearson.  The  repression  of  tuberculosis  of  cattle  by  sanita- 
tion.    Bulletin  77.     Penn.  Dept.  of  Agric.     1901. 

11.  Ravenel.  The  dissemination  of  tubercle  bacilli  by  cows  in 
coughing  a  possible  source  of  contagion.  Univ.  of  Penn.  Med.  Mag- 
azine.    Nov.      19C0. 

12.  Ravenel.  The  comparative  virulence  of  the  tubercle  bacillus 
from  human  and  bovine  sources.    Univ.  of  Penn.  Med.  Bui.    Sept.,  1901. 

13.  Ravenel.  The  intercommunicability  of  human  and  bovine 
tuberculosis.      The  Univ.  of  Penn.  Medical  Bulletin.     May.     1902. 

14  Repp.  Transmission  of  tuberculosis  through  meat  and  milk. 
American  Medicine.     Oct.  6,  Nov.  2.     1901. 

15.  Salmon.  Legislation  with  reference  to  bovine  tuberculosis. 
Bulletin  28.     U.  S.  Dept.  of  Agr.  Bureau  of  Animal  Industry.     1901. 

16.  Salmon.  The  tuberculin  test  of  imported  cattle.  Bulletin  32. 
Bureau  of  Animal  Industry.  U.  S.  Dept.  of  Agr.     1901. 

17.  Smith.  Investigations  concerning  bovine  tuberculosis  with 
special  reference  to  diagnosis  and  prevention.  (Pathological  part). 
Bulletin  No.  7.,  U.  S.  Dept.  of  Agr.  Bur.  of  Animal  Industry.     1894. 

18.  Smith.  A  comparative  study  of  bovine  tubercle  bacilli  and  of 
human  bacilli  from  sputum.      The  four,  of  E.vper.  Med.    Vol.  III.     1898. 

19.  Smith.  The  thermal  death  point  of  tubercle  bacilli  in  milk 
and  some  other  fluids,    four.  Experimental  Med.  Vol.  IV.   No.  2.   1S99. 

The  following  bulletins  on  tuberculosis  have  been  issued 
from  the  various  State  Agricultural  Experiment  Stations  : 

Bitting.  Bovine  tuberculosis  in  Indiana.  (Purdue).  Bui.  63. 
Ind.     1896. 

Brewer.     Tuberculosis.     Bui.  41.     Utah.     1S95. 

Gary.     Bovine  tuberculosis.     Bui.  67.     Alabama.      1895. 

Fischer.     Bovine  tuberculosis.     Bui.  79.     Kansas.     1898. 

Grange.     Tuberculosis.     Bui.  133.     Mich.     1896. 

Hills  and  Rich.     Bovine  tuberculosis.     Bui.  42.     Vermont.    1894. 

Law.  Tuberculosis  in  relation  to  animal  industry  and  public 
health.     Bui.  65.      (Cornell.)     New  York.      1S94. 

Law.  Experiments  with  tuberculin  on  non-tuberculous  cows.  Bui. 
82.      (Cornell.)     New  York.     1894. 

Law.    Tuberculosis  in  cattle  and  its  control.  Bui.  150.  Cornell.   1898. 

Marshall.  A  study  of  normal  temperatures  and  the  tuberculin 
test.     Bui.  159.     Michigan.      189S. 

Marshall.  Killing  the  tubercle  bacilli  in  milk.  Bui.  173.  Michi- 
gan.    1S99. 

Mavo.     Some  diseases  of  cattle,  Texas  itch,  blackleg,  tuberculosis, 

Texas  fever.     Bui.  69.     Kansas.     1897. 

Nelson.  On  the  use  of  Koch's  lymph  in  the  diagnosis  of  tubercu- 
losis.    Report  of  the  biologist.     New  Jersey.      1S93. 


OVINE    CASEOUS    LYMPH-ADENITIS  l6l 

Nelson.  Experitnental  studies  of  the  Koch  test  for  tuberculosis. 
New  Jersey.      1S95. 

Nelson.  The  suppression  and  prevention  of  tuberculosis  of  cattle 
and  its  relation  to  human  consumption.     Bui.    118.     New  Jersey.      1896. 

Nesom.     Tuberculosis  of  cattle.     Bui.  50.     vS.  C.      1900. 

Pe.\RSON.     Tuberculosis  of  cattle.     Bui.  29.     Penn.      1894. 

Russell.  Tuberculosis  and  the  tuberculin  test.  Bui.  40.  Wiscon- 
sin.     1894. 

Russell.  The  history  of  a  tuberculous  herd  of  cows.  Bui.  78. 
Wisconsin.      1899. 

Russell  and  Hastings.  Bovine  tuberculosis  in  Wisconsin.  Bui. 
S4.     Wisconsin.      1901. 

Stalker  and  Niles.  Investigation  of  bovine  tuberculosis  with 
special  reference  to  its  existence  in  Iowa.     Bui.  29.     Iowa.      1S95. 

Thorne.     Bovine  tuberculosis.     Bui.  loS.     Ohio.      1899, 

Williamson  and  Emery.  Tuberculosis  and  its  prevention.  Bui. 
117.     N.  C.     1895. 


OVINE    CASEOUS    LYMPH-ADENITIS.     (PSEUDO    TUBER- 
CULOSIS IN  SHEEP.) 

§  iig.  Characterization.  Caseous  lymph-adenitis  is  a 
disease  of  aduh  sheep  which  iiutil  recently  was  designated  as 
pseudo-tuberculosis.  It  has  been  characterized  by  an  enlarge- 
ment of  one  or  more  lymphatic  glands  which  contain  foci 
of  a  greenish-yellow,  caseous  or  purulent  substance.  It  is 
rarely  found  in  young  animals.  The  mortalit}'  is  very  low 
due,  perhaps,  to  the  fact  that  the  sheep  are  slaughtered  before 
the  disease  has  time  to  develop.  It  does  not  occur  in  epizootic 
form  although  it  is  more  prevalent  in  certain  localities  than  in 
others. 

^  120.  History.  The  name  "Ovine  Caseous  Lymph  Aden- 
itis'' was  proposed  by  Norgaard  and  Mohler  in  1899.  These 
writers  found  the  lesions  and  the  accompanying  microorganism 
to  correspond  with  those  described  by  Preisz  and  Guinard  in 
1 89 1  as  pseudo-tuberculosis.  The  bacterium  was  fully  described 
by  Preisz  in  1894.  The  organism  has  been  found  and  identified 
from  a  lai-ge  variety  of  lesions  in  a  number  of  species  of  ani- 
mals. It  appears  that  at  least  many  of  the  cases  of  lymphatic 
gland  enlargement  heretofore  called  pseudo-tuberculosis  in 
sheep  belong  to  this  disease.  Cherry  and  Bull  describe  it  as 
caseous  lymphatic  glands  and  Sivori  as  caseous  broncho-pneu- 
monia ;  the  bacterium  of  Preisz  being  found  as  the  probable 
cause  in  each  case. 


1 62  OVINE    CASEOUS    LYMPH-ADENITIS 

§121.  Geographical  distribution.  In  the  United  States 
this  disease  is  quite  common  in  certain  districts  in  the  western 
and  southwestern  states.  It  exists  in  South  America,  Aus- 
tralia and  Europe. 

Sivori  found  that  lo  per  cent  of  the  old  sheep  killed  in 
Buenos  A^'res  were  affected.  The  prevalence  of  the  disease  in 
the  United  States,  as  indicated  b}'  the  reports  of  the  federal 
meat  inspectors,  show  that  of  16,000,000  sheep  slaughtered  in 
Chicago,  Kansas  Cit}'  and  South  Omaha  3,236  were  con- 
demned for  caseous  lymph  adenitis  or  lesions  which  might  be 
confounded  with  it.  It  is  reported  by  an  inspector  from  Los 
Angeles  that  of  950  sheep  coming  from  an  infected  district,  82 
were  suffering  from  lymph  adenitis. 

§122.    Etiology.    Caseous  lymph  aden- 
itis is  caused  by  a  specific  organism.      It  ap- 
pears to  be  the  one  described  first  by  Preisz 
as  the  bacillus  of  pseudo-tuberculosis.     Its 
description  shows  it  to  vary  in  size  to  such 
a  degree  that  its  polymorphism  is  said  to  be 
characteristic.    It  is  nonmotile  and  hence  be- 
longs to  the  genus  Baderinm.     It  is  aerobic, 
facultative   anaerobic,  it   stains  readily  and   does   not  produce 
spores.    It  develops  readily  on  agar  when  this  medium  is  inocu- 
lated from  the  caseous  material   from  the  affected  glands.      It 
is  pathogenic  for  mice,  guinea  pigs  and  rabbits. 

§  123.  Symptoms.  In  the  majority  of  cases  no  symp- 
toms of  any  importance  are  observed  in  the  affected  animals 
during  life.  The  course  of  the  disease  is  that  of  a  chronic 
affection  and  the  pathological  changes  develop  so  slowly  that 
no  general  or  local  interference  with  the  health  of  the  affected 
animals  are  observed,  in  lambs  and  sheep  that  are  bred  and 
raised  for  mutton,  and  which  are  marketed  before  they  are 
two  years  old.  Only  in  breeding  ewes  and  wethers  does  the 
disease  advance  to  a  degree  which  makes  it  clinicalh'  recog- 
nizable without  the  aid  of  manipulation.  The  affected  ani- 
mals upon  examination  show  an  enlargement  of  one  or  more 
of  the  superficial  glands,  the  precrural  and  the  sub-scapular 
glands  being  most  often  involved.     The  animals  thus  affected 


-'• 

« 

# 

Fig 

•37- 

Bac 

-tei 

-2uin 

of  Preisz. 

SYMPTOMS  163 

appear  iu  everj-  other  respect  to  be  in  perfect  health.  In  the 
older  animals — the  wethers  and  breeding  ewes — the  same 
glands  may  be  enlarged  to  a  considerable  degree  reaching  the 
size  of  a  hens  egg  or  even  larger.  Some  of  these  sheep  may 
show  a  certain  degree  of  unthriftiness  or  even  emaciation. 
The  disease  is  found  in  its  most  advanced  stages  in  the  older 
ewes,  which  is  probably  due  to  the  fact  that  the  wethers  are 
generally  disposed  of  before  they  are  three  years  old,  while  a 
good  breeding  ewe  is  frequently  retained  for  seven  or  eight 
years.  In  such  old  animals  the  superficial  lymphatic  glands 
may  be  enlarged  to  such  a  degree  as  to  interfere  with  locomo- 
tion, while  the  deeper  seated  glands  and  those  of  the  body 
cavities  are  similarly  affected.  In  the  advanced  cases  the 
lesions  often  become  disseminated  by  metastasis  to  the  princi- 
pal organs  of  the  body.  In  such  cases  the  disease  maj'  assume 
the  appearance  of  chronic  broncho-pneumonia  or  pleuris}-, 
with  occasional  cough,  slight  dyspnoea  and  increasing  emacia- 
tion and  ansemia.  The  course  of  the  disease  is  exceedingly 
slow.  For  this  reason  owners  of  affected  flocks  are  often 
totally  ignorant  of  the  presence  of  the  disease.  This  fact  ren- 
ders it  verj^  difficult  to  obtain  reliable  information  regarding 
its  prevalence  save  from  the  statistics  obtained  from  the 
slaughter  houses.  A  majorit\'  of  the  inspectors  have  until 
recently  classified  the  lesions  either  as  tuberculosis,  pyemia  or 
abscesses.  In  response  to  inquiries  it  was  found  that  the  ma- 
I'ority  of  cases  which  had  been  condemned  under  these  head- 
ings were  undoubtedly  caseous  lymphadenitis.  Several 
thousand  cases  are  annually  observed  in  the  slaughter  houses 
of  the  United  States,  but  only  a  fraction  of  these  are  advanced 
to  a  degree  that  would  warrant  a  total  condemnation  of  the 
carcasses.  Meat  inspectors  agree  that  lambs  are  very  rarely 
affected,  and  that  the  progress  of  the  morbid  changes  in  the 
majority  of  cases  is  coordinate  with  the  age  of  the  animal. 

§  124.  Morbid  anatomy.  The  principal  lesions  are 
confined,  according  to  the  various  descriptions,  especially  that 
by  Norgaard  and  Mohler,  to  the  lymphatic  glands.  In  many 
cases  only  a  single  gland  is  affected.  The  relative  frequency 
with  which  the  various  glands  become   the  seat  of  the  lesions 


164  OVINE    CASEOUS    LYMPH-ADENITIS 

may  be  given  as  follows  :  prescapular,  precrural,  superficial 
inguinal,  bronchial,  mediastinal,  sub-lumbar,  deep  inguinal, 
and  scrotal.  Rarel}'  the  suprasternal  and  mesenteric  glands 
are  affected.  Sivori  mentions  the  mesenteric  glands  among 
those  frequently  affected.  He  fails,  however,  to  mention  the 
mesenteric  glands  as  the  seat  of  lesions  in  the  detailed  descrip- 
tion of  twelve  typical  cases  of  caseous  broncho-pneumonia 
caused  by  the  bacillus  of  Preisz. 

When  first  invaded  b^^  the  bacterium,  the  adenoid  tissue 
becomes  h3'perplastic  and  the  gland  enlarges  to  several  times 
its  original  size.  On  section,  the  surface  is  found  to  be  waterj^ 
but  otherwise  the  tissue  retains  its  normal  appearance.  This 
is  followed  by  the  formation  of  various  centers  of  degeneration 
which  show  concentric  layers  and  gradually  become  confluent. 
Finally,  the  total  volume  of  the  gland  is  transformed  into  a 
homosreneous  caseous  mass.  At  the  same  time  the  distended 
capsule  increases  in  thickness  and  forms  a  sac  which  confines 
the  semifluid,  grumous  mass.  In  rare  instances  the  sac  rup- 
tures and  when  close  to  the  surface  the  contents  will  be  dis- 
charged. Under  ordinary  circumstances,  the  caseous  contents 
become  cohesive  and  sticky  and  of  the  consistency  of  putty. 
In  very  old  cases  the  mass  becomes  drj-  and  mealy  with  little 
or  no  tendency  to  calcification.  The  greenish  yellow  color  of 
the  caseous  mass,  which  is  stated  to  be  most  characteristic, 
closeh'  resembles  the  contents  of  the  intestinal  nodules  pro- 
duced b}"  Oesophagostoma  Columbianum.  In  very  advanced 
cases,  as  for  instance  those  of  old  breeding  ewes,  the  internal 
organs  may  contain  lesions  which  microscopically  resemble 
those  of  tuberculosis.  The  lungs  may  be  studded  with  small 
nodules  the  size  of  a  pea,  the  spleen,  liver  and  in  rare  in- 
stances the  kidneys  also  may  contain  one  or  more  foci  of  the 
same  character,  namely,  a  mass  of  greenish  yellow  material, 
surrounded  by  a  firm,  fibrous  sac.  There  seems,  however,  to 
be  a  distinct  line  of  demarcation  between  the  affected  and  the 
healthy  tissue.  There  is  no  indication  of  an  inflammatory  zone. 
The  bronchial  and  the  mediastinal  glands  may  be  affected  to  a 
considerable  extent  without  any  lesions  being  found  in  the 
lungs.      In  some  cases  the  lungs  are  extensively   involved. 


MORBID    ANATOMY  I  65 

The  lesions  consist  of  nodules  varying  in  size  from  that  of  a 
millet  seed  to  that  of  a  walnut.  This  condition  is,  as  a  rule, 
accompanied  by  a  chronic  pleurisy  with  extensive  adhesions 
and  also  effusions  into  the  plural  cavities. 

In  the  liver  the  lesions  consist  largely  of  nodules  com- 
posed like  those  in  the  lymphatic  glands,  of  a  firm  white 
fibrous  sac  containing  a  greenish-yellow,  cheesy  mass  of  vary- 
ing consistenc}'.  Cases  have  been  reported,  however,  where 
the  entire  organ  was  filled  with  miliary  nodules. 

The  kidneys  are  rarely  affected  but  when  they  are  the 
lesions  assume  the  same  characteristic  appearance  of  a  firm 
walled  abscess  protruding  on  the  surface  of  the  organ.  As  a 
rule,  only  one  or  two  such  foci  are  observed  in  each  case. 

A  histological  examination  of  tissue  containing  miliary  or 
sub-miliary  nodules,  show  them  to  be  composed  chiefly  of 
leucocytes  and  nucleated  round  cells,  the  greater  part  of  which 
are  irregular  in  shape,  especially  toward  the  center  where 
many  of  them  are  transformed  into  a  granular  detritus.  Among 
the  cells  singly  or  arranged  in  clumps,  are  seen  the  short 
plump  bacteria  which  stain  irregularl}-.  The  shape  varies 
considerably  from  oval  or  oblong  to  dumb-bell  and  club  shape. 

The  bacteria  are  frequently  seen  within  the  degenerated 
leucocytes,  the  destruction  of  which  is  due,  according  to 
Preisz,  to  the  specific  chemical  products  elaborated  by  these 
microorganisms. 

The  microscopic  appearance  is  somewhat  similar  in  all  the 
lesions  whether  located  in  the  lymph  glands,  lungs,  liver,  kid- 
neys or  spleen.  In  the  lungs  the  histological  picture  re- 
sembles that  of  broncho-pneumonia.  In  the  liver  the  lesions 
originate  in  the  portal  capillaries,  where  the  bacteria  cause  a 
proliferation  of  the  endothelial  cells,  which,  together  with  the 
accumulation  of  leucocytes  and  red  blood  corpuscles,  cause  the 
obliteration  of  the  vessels.  In  no  case  have  giant  cells  been 
observed.  The  surrounding  hepatic  cells  become  swollen, 
then  granular  and  finally  the}'  undergo  atrophy,  leaving  open 
spaces  between  them.  Numerous  round  cells  appear  in  the 
periphery  of  the  nodules  which  gradually  undergo  a  connective 


1 66  OVINE    CASEOUS    LYMPH-ADENITIS 

tissue   metamorphosis  and  become   organized   into  an  encap- 
sulating membrane. 

When  a  miliary  nodule  from  the  liver  of  an  experimental 
animal  which  has  been  destroyed  three  weeks  after  inoculation 
is  examined  microscopicalh^  the  following  picture  is  observed. 
A  caseous  center  composed  of  an  amorphous  material  that 
does  not  take  any  of  the  ordinar}'  stains.  Surrounding  the 
center  ma}-  be  seen  numerous  leucocytes  more  or  less  degener- 
ated and  frequently  containing  one  or  more  bacteria  while 
clumps  of  these  organisms  are  scattered  among  them.  Ex- 
ternal to  this  is  a  dense  round  cell  infiltration  the  peripheral 
zone  of  which  is  undergoing  connective  tissue  formation  thus 
serving  as  a  line  of  demarcation  between  the  atrophied  liver 
cells  and  the  central  cell  ma.ss.  The  process  then  repeats  itself 
until  a  connective  tissue  barrier  strong  enough  to  encapsulate 
the  central  part  of  the  nodule  and  prevent  its  further  growth 
is  obtained.  The  nodules  in  the  kidneys  and  lungs  present  a 
similar  microscopic  appearance,  excepting  that  the  foci  in  the 
lungs  are  more  regular  on  account  of  the  catarrhal  inflamma- 
tion that  accompanies  the  reaction  of  the  surrounding  tissue. 
The  center  contains  a  dense  mass  of  disintegrated  cell  structures 
composed  of  the  desquamated  and  proliferated  epithelial  cells, 
degenerated  leucocytes  and  round  cells.  In  experimental 
animals  which  succumb  quickly  to  an  intravenous  injection  of 
virulent  material,  the  lung  tissue  immediately  surrounding  the 
nodules  is  frequently  seen  to  be  hepatized. 

§  125.  Differential  diagnosis.  This  specific  lymphatic 
affection  is  to  be  differentiated  from,  (i)  other  infections  which 
may  cause  enlargement  or  suppuration  of  lymph  glands,  and 
(2)  tuberculosis.  If  the  diagnosis  cannot  be  made  from  the 
gross  appearance  of  the  lesions  a  bacteriological  examination 
will  be  necessar}'.  The  fact  should  be  kept  in  mind  that 
tuberculosis  in  sheep  is  ver}-  rare.  With  lymph-adenitis, 
cultures  in  ordinary  media  will  give  a  growth  of  the  bacterium 
of  Preisz.  With  tuberculosis  the  result  would  be  negative. 
(See  tuberculosis)  It  is  important  not  to  confuse  the  nodular 
disease  of  sheep's  intestines  with  this  affection.     The  location 


ASTHENIA    IN    FOWLvS    AND    PIGEONS  1 67 

of  the  lesions  in  the  walls  of  the   intestine  will  be   quite  suffi- 
cient to  determine  the  nodular  disease. 

REFERENCES. 

1.  Cherry  and  Bull.  Caseous  lymphatic  glands  (pseudo-tubercu- 
losis) in  sheep.      The  Veterinarian.     Vol.  LXXII.     p.  523- 

2.  Eberth,  C.  J.  Bacillare  Nekrose  der  Leber.  Vtrchow's  Arcfiiv., 
Bd.  C.     (i8S5)p.'23. 

3.  Norgaard  and  Mohlkr.  The  nature,  cause,  and  economic 
importance  of  ovine  caseous  lymph-adenitis.  Sixteenth  Annual  Report, 
Bureau  of  Animal  Industry.     1S99.  p.  638.     (Full  bibliography). 

4.  Preisz  and  Guinard.  Pseudo-tuberculose  chez  le  mouton. 
/ourn.  de  med.  de  vet.  et  de  zodtech.  ser.  3,  Vol  XVI.     ( 1S91)  p.  563. 

5.  Preisz.  Recherches  comparatives  sur  les  pseudotuberculoses 
bacillaires  et  une  nouvelle  espec  de  pseudotuberculose.  Ann.  de  V Inst. 
Pasteur,  Vol.  VIII.     {1S94)  p.  231. 

6.  SivoRi.  Sur  une  broncho-pneumonie  caseouse  du  mouton,  causee 
par  le  bacille  de  Nocard-Preisz.  Rev.  de  vied.  vet.  ser.  8,  Vol.  VI. 
(1S99)  p.  657.  

ASTHENIA  IN  FOWLS  AND  PIGEONS. 

§126.  Characterization.  This  is  a  disease  especially 
of  chickens  and  pigeons  in  which  there  is  marked  emaciation 
and  a  failure  to  take  on  flesh  even  when  fed  on  the  most 
nourishing  food.  Because  of  this,  the  disease  has  received  the 
popular  name  of  "going  light." 

§  127.  History.  Although  this  condition  or  disease  has 
been  recognized  for  a  long  time  it  seems  to  have  been  first 
described  in  1898  by  Dawson.  He  gives  a  brief  account  of  the 
symptoms,  morbid  anatomy,  etiology  and  a  somewhat  ex- 
tended description  of  the  specific  organi.sm  which  he  isolated 
from  the  diseased  chickens.  The  writer  has  studied  this 
affection  in  pigeons  but  did  not  succeed  in  finding  the  organism 
isolated  by  Dawson. 

§  128.      Etiology.     Dawson    found  this  ^^^^^^^    ^ 

disease  to  be  due  to  the  presence  of  a  certain  ^^  ^ 

species  of  bacterium  which  he  obtained  in  ^  ^  ^ 
pure  culture  from  the  duodenal  contents.  He 
described  it  as  Baderhwi  asthenice.  This 
organism  varies  from  i  to  1.3//  in  length  and 
about  0.5// in  width  with  rounded  ends.  It  Fig.  38.  Bacter- 
is  reported  to  possess  the  peculiarity  of  vege-  ///;;/  as  the  n  ice. 
tating  in   temperatures  varying   from   50  to    [Dawson.) 


1 68  ASTHENIA    IN    FOWLS    AND    PIGEONS 

1 20°  F.  It  is  fatal  to  rabbits  within  24  hours  when  inoculated 
into  the  abdominal  cavit}'  w-ith  0.5  c.  c.  of  a  bouillon  culture. 
Chickens  inoculated  with  this  organism  remained  well. 

§  129.  Symptoms.  The  only  symptoms  which  seem  to 
be  in  evidence  are  the  gradual  loss  of  flesh  and  an  exceedingly 
good  appetite.  It  is  reported  by  certain  pigeon  fanciers  con- 
cerning pigeons  and  the  fact  is  reiterated  by  Dawson,  that  the 
disease  is  an  exceedingly  chronic  one,  often  extending  over  a 
period  of  several  months  but  usually  terminating  in  death. 
In  the  cases  reported,  the  fowls  were  well  kept  and  given  an 
abundance  of  nourishing  food.  There  seems  to  be  an  inability 
on  the  part  of  the  affected  animal  to  assimilate  nourishment. 

§  130.  Morbid  anatomy.  The  most  conspicuous  lesion 
is  extreme  emaciation.  According  to  Dawson  the  mucosa  of 
the  duodenum  contains  areas  in  which  the  walls  are  deeply 
reddened  and  in  which  the  contents  are  of  a  mucoid  substance. 
The  writer  made  a  number  of  post-mortems  in  pigeons  suffer- 
ing from  this  disease  without  finding  any  gross  tissue  changes. 

This  disease  needs  further  investigation  but  the  fact  that 
an  organism  has  been  found  in  the  duodenum  in  large  numbers 
wl^ere  it  multiplies  and  apparently  produces  by-products  that 
are  absorbed,  and  which  interfere  with  the  normal  metabolism 
of  the  body,  is  of  sufficient  interest  to  call  attention  to  the 
preliminary  findings  herein  mentioned.  It  is  not  unlikeh- 
that  if  the  present  hypothesis  concerning  the  nature  of  this 
disease  is  verified  that  a  number  of  disorders  now  attributed 
to  general  causes  may  be  traced  to  some  form  of  intestinal 
infection. 

REFERENCES. 

I.  Dawson.  .Asthenia  (going  light)  in  fowls.  Annual  Report 
of  the  Bureau  of  Animal  Industry  U.  S.  Department  of  Agriculture^ 
1898.     p.  329. 


CHAPTER    IV. 


DISEASES  CAUSED  BY  BACTERIA— GENUS  BACILLUS. 


HOG  CHOLERA. 


Synonyms.*  Swine  fever  ;  Pneumo-enteritis  ;  Pig  ty- 
phoid ;  Svinpest. 

§131.  Characterization.  The  distinguishing  features 
of  this  disease  are  a  continuous  fever,  ulceration  of  the  intes- 
tines, and  more  or  less  discoloration  of  the  skin,  especially 
over  the  ventral  surface. 

§  132.  History.  The  earliest  outbreak  in  this  country  of 
which  there  is  knowledge  of  a  disease  supposed  to  be  hog 
cholera  occurred  in  the  state  of  Ohio  in  1833.  It  is  presumed 
that  it  was  brought  from  Europe  with  some  of  the  animals 
imported  from  there  for  breeding  purposes.  After  being  intro- 
duced, it  spread  at  first  slowly,  but  later  with  increasing 
rapidity  along  the  lines  of  commerce,  until  it  invaded  every 
part  of  this  country  where  swine  raising  had  become  an 
industry.  The  disease  was  investigated  and  very  carefully 
described  by  Dr.  C.  Sutton  of  Aurora,  Ind.,  from  1850. to 
1858.  In  1861,  Dr.  Edwin  M.  Snow,  of  Providence,  R.  I., 
contributed  an  important  paper  on  this  disease  to  the  U.  S. 
Department  of  Agriculture.  In  1875,  Dr.  James  Eaw,  of 
Ithaca,    N.  Y. ,  furnished    to    the  same  Department    a   paper 


*This  disease  is  known  popularly  by  a  large  number  of  names  and 
in  some  works  on  swine  diseases  many  of  them  are  employed.  The 
more  common  of  these  are,  enteric  fever,  typhus  carbuncular  fever,^ 
carbuncular  gastro-enteritis,  carbuncular  typhus,  pig  distemper,  blue 
sickness,  blue  disease,  purples,  red  soldier,  anthrax  fever,  scarlatina, 
measles,  diphtheria,  and  erysipelas.  Many  of  the  terms  appear  to  refer 
to   some  one  or  more  of  the  observed  symptoms  or  lesions. 


lyo  HOG    CHOLERA 

setting  forth  the  symptoms  and  morbid  anatom\-  of  this 
disease.  He  beheved  it  to  be  contagious  although  the  specific 
organism  had  not  been  found.  The  U.  S.  Commissioner  of 
Agriculture  appointed,  in  1878,  nine  men  for  a  period  of  two 
months  each  to  investigate  the  disease  in  various  localities. 
In  their  reports  the  symptoms  and  morbid  anatomy  formerl}' 
described  were  confirmed  and  two  additional  features  set 
forth.  Law  showed  that  it  was  transmissible  by  inoculation  to 
other  animals  (rabbits,  rats  and  sheep)  and  Dr.  Detmers 
described  a  microorganism  which  he  called  Bacilhis  siiis  and 
which  he  believed  to  be  the  specific  cause  of  the  trouble. 
Later,  Detmers  described  his  organism  as  a  micrococcus. 
The  transmission  of  the  malady  to  rats  and  sheep  was  not 
confirmed  by  subsequent  tests.  The  work  of  investigation  was 
continued  under  the  direction  of  the  Commissioner  of  Agri- 
culture and  finally,  in  1885,  the  specific  organism  was 
discovered  by  Salmon  and  Smith,  who  described  its  essential 
characters  and  properties.  It  was  called  Bacterium  of  swine 
plague.  Since  that  time  the  disease  has  been  under  investiga- 
tion and  the  Bureau  of  Animal  Industry  has  during  the  last 
few  3'ears  been  actively  engaged  in  the  effort  to  produce  a 
specific,  therapeutic  serum. 

In  1 886,  Dr.  Theobald  Smith  discovered  another  bacterial 
disease  among  swine.  It  was  found  to  be  similar  to  the  Ger- 
man Sdrcccincseuche,  both  in  its  morbid  anatomy'  and  in  the 
morphology  and  properties  of  its  specific  organism  (see  §  47). 
In  naming  this  disease  the  Bureau  of  Animal  Industry  called 
it,  on  account  of  its  similarity  to  the  German  Schwemeseuche, 
swine  plague  and  its  organism  the  bacillus  of  swine  plague, 
and  changed  the  name  of  the  disease  described  in  1885  to  hog 
cholera  and  its  organism  to  the  bacterium*  of  hog  cholera. 
The  changing  of  the  name  of  the  first  disease  described  from 
swine  plague  to  hog  cholera  has  been  the  cause  of  some  criti- 
cism and  it  has  been  credited  with  the  responsibility  of  creat- 
ing confusion.  It  has,  perhaps,  led  hasty  readers  to  a  misin- 
terpretation of  these  diseases  and  their  relation   to    those  des- 


*In    188S   the  genus  Bacterium  was  changed  to  Bacillus  and   this 
organism  is  spoken  of  since  that  time  as  the  hog-cholera  bacillus. 


ETIOLOGY  lyr 

cribed  in  other  lands  under  different  titles.  While  the  names 
assigned  may  not  have  been  especially  happy  ones,  the  trans- 
fer of  swine  plague  from  the  intestinal  to  the  lung  disease 
must  be  considered  as  a  fortunate  occurrence  and  one  which 
tended  to  simplify  and  not  to  confuse. 

Billings,  of  the  Nebraska  State  Experiment  Station, 
opposed  this  nomenclature.  He  not  only  refused  to  accept 
the  change  and  continued  to  write  about  hog  cholera  under 
the  title  of  swine  plague,  but  he  denied  the  existence  of  the 
swine  plague,  as  described  in  the  reports  of  the  Bureau  of 
Animal  Industry  for  1886  and  subsequently,  as  an  indepen- 
dent disease.  The  wide  dissemination  of  his  publications  on 
this  subject  has  unquestionably  been  responsible  for  much  of 
the  haziness  concerning  the  distinguishing  features  of  these 
maladies. 

In  1893,  Drs.  Welch  and  Clements  read  a  paper  before  the 
International  Veterinary  Congress  in  which  they  gave  a  very 
clear  history  of  the  nomenclature  of  these  diseases  and  in 
which    they    adhered    to    the   one   of  the  Bureau  of  Animal 

Industry. 

§133.  Geographical  distribution.  Hog  cholera  is  widely 
disseminated  throughout  the  central  part  of  the  United  States. 
It  exists,  however,  to  a  certain  degree  in  every  state  in  the 
Union  and  in  Canada.  It  has  long  been  known  in  Great 
Britain.  It  prevails  to  a  greater  or  less  extent  on  the  European 
continent.  The  confu.sion  which  has  arisen  in  the  use  of  the 
terms  swine  plague  and  hog  cholera  renders 
it  difficult  to  determine  from  the  brief  de- 
scription in  a  number  of  reports  the  nature 
of  the  malady  in  question.  .^ 

§134.     Etiology.    The  specific  disease,  Sk;^  ^1 

here  described  as  hog  cholera,  is  caused  by  . 

°  .  .     .  Fig.  39.  Bacillus 

Bacillus  cholerae  suis.      A  brief  description  of  hog  cholera  both 

of  its  morphology,  physiological  properties  with    and    ivithoid 

and  pathogenesis  are  appended.  flagella. 

^  135.      A    brief   description    of   the  bacillus    of   hog 
cholera. 


172  HOG    CHOLERA 

Morphology. — A  rod-shaped  organism  varying  in  size  according  to 
the  medium  in  which  it  has  developed.  From  agar  cultures  it  is  from 
1.2  to  1.8/-/  long  and  from  .5  to  .8//  broad.  The  ends  are  rounded. 
Spores  have  not  been  observed.  It  is  actively  motile  and  a  variable 
number  but  usually  from  3  to  5  flagella  have  been  demonstrated.  The 
length  of  the  flagella  also  varies.  The  average  seems  to  be  about  7//  — 
although  filaments  55  microns  with  an  average  length  of  35  to  40//  are 
reported  by  Ferrier.  It  stains  readily  with  the  aniline  dyes.  Prepara- 
tions made  from  cultures  usually  stain  uniformly  ;  while  in  the  prepara- 
tions made  from  the  tissue  of  inoculated  animals  there  is  frequently 
exhibited  a  light  center  with  a  deeply  stained  peripherj'. 

Cultural  characters  and  biochemic  properties. — This  bacillus  is 
grown  readily  on  all  of  the  ordinary  media  used  in  bacteriological  work 
at  a  temperature  of  30  to  38°  C.     It  is  aerobic  and  facultative  anaerobic. 

Agar. — On  the  surface  of  inclined  agar  after  24  hours  at  a  tempera- 
ture of  37°  C.  a  grayish,  glistening  nonviscid  growth  appears.  When 
isolated  the  colonies  are  nearly  round,  convex,  0.5  to  2.0  mm.  in 
diameter.  The  edges  are  sharply  defined  and  even.  In  stab  cultures  a 
grayish  growth  develops  along  the  needle  track  with  a  more  vigorous 
growth  on  the  surface  about  the  needle  puncture.  The  growth  reaches 
its  maximum  in  about  48  hours. 

Gelatin. — In  this  medium  the  growth  is  moderately  feeble,  the 
colonies  appearing  as  grayish  dots.  When  magnified  they  are  finely 
granular  and  of  a  yellowish  tint.  The  quantity  and  form  of  growth 
depends  considerably  upon  the  reaction  of  the  gelatin.  If  decidedlj' 
alkaline  there  is  often  a  tendency  for  the  growth  to  spread.  There  is  no 
softening  or  liquefaction  of  the  medium. 

Potato. — The  growth  on  potato  takes  the  form  of  a  verj-  thin,  glisten- 
ing layer.  It  is  usually  of  a  faintly  yellowish  color  but  this  is  subject 
to  variation  on  different  potatoes.  If  the  reaction  is  strongly  acid  no 
growth  appears. 

Bouillon. — In  alkaline  bouillon  it  imparts  in  24  hours  a  uniformly 
■cloudy  appearance  to  the  liquid.  Ordinarily  there  is  no  membrane  on 
the  surface.  After  some  days'  standing  the  growth  begins  to  settle, 
forming  a  grayish,  friable  sediment.  If  the  bouillon  contains  muscle 
sugar  the  reaction  will  be  changed  to  acid,  in  from  24  to  48  hours,  due 
to  the  fermentation  of  the  sugar.  Later,  however,  the  liquid  will 
become  strongly  alkaline,  unless  there  was  too  much  muscle  sugar  pres- 
ent. In  acid  bouillon  the  growth  is  less  vigorous.  It  grows  better  in  a 
bouillon  containing  peptone  than  in  a  simple  beef  broth. 

Milk. — When  the  milk  is  acid  in  the  beginning  it  gradually  becomes 
alkaline.  There  is  no  precipitation  or  coagulation  of  the  casein.  After 
standing  for  from  two  to  three  weeks  in  an  incubator  a  gradually 
developing  opalesence  of  the  milk  can  be  observed.  Later  it  becomes 
clear,  then  light  brownish  in  color.  If  allowed  to  stand  longer  in  the 
incubator   the  volume  of   the  culture  shrinks  by  evaporation  and  the 


ETIOLOGY  173 

opalescent  liquid  becomes  quite  thick  and  dark-colored  but  not  viscid. 
When  the  opalesence  appears  the  milk  is  strongly  alkaline.  The  pro- 
cess seems  to  be  a  form  of  saponification  of  the  fat  globules  due  to  the 
presence  of  the  alkali  produced  by  the  bacteria. 

Indol. — In  Dunham's  solution  the  growth  is  quite  feeble.  Ordi- 
narily no  indol  reaction  is  obtained  although  it  has  been  observed  in 
a  few  cultures  obtained  from  different  epizootics. 

Gas  production. — In  peptonized  bouillon  containing  i  per  cent, 
dextrose,  gas  appears  within  24  hours  and  continues  to  form  for  from 
three  to  five  days.  During  the  first  day  from  one-fourth  to  one-half  of 
the  total  quantity  is  produced.  By  the  end  of  the  second  day  the  gas 
formation  is  nearly  at  an  end.  The  total  amount  which  collects  in  the 
closed  branch  of  the  fermentation  tube  is  equivalent  to  about  one-half 
of  the  capacity  of  this  branch.  The  gas  set  free  is  composed  of  CO^  and 
an  explosive  gas  which  consists  largely  of  H.  The  ratio  of  CO,  to  H  in 
the  fermentation  tube  is  approximately  as  i  :2.  The  reaction  of  the  liquid 
becomes  strongly  acid,  which  condition  checks  the  multiplication  of  the 
bacteria. 

Gas  is  not  produced  in  bouillon  containing  lactose  or  saccharose. 
These  sugars  are  not  fermented.  Alkaline  cultures  containing  them 
become  more  strongly  alkaline  as  the  growth  continues. 

Thermal  reactions. — This  organism  grows  very  feebly  at  a  tem- 
perature of  20°  C.  It  will  not  thrive  at  a  temperature  above  43°  C.  It 
is  destroyed  when  exposed  to  moist  heat  at  58°  C.  for  10  minutes. 

Disinfectants. — This  organism  is  destroyed  after  an  exposure  for  10 
minutes  or  less  in  the  following  solutions: 

Carbolic  acid,  i  per  cent.  Hydrochloric  acid,  1-5  of  i  per  cent. 
Sulphuric  acid,  1-20  of  i  per  cent.  Sulphate  of  copper,  1-4  of  i  per  cent. 
Formalin,  i  to  2,000.     Trikresol,  1-2  of  i  per  cent. 

Lime  is  also  a  good  disinfectant  when  used  in  preparations  contain- 
ing about  I  per  cent  CaO. 

Drying. — This  bacillus  resists  drying  for  a  variable  length  of  time, 
according  to  the  amount  of  protection  it  has.  In  a  drop  of  a  bouillon 
culture  dried  on  a  cover-glass  and  kept  under  bell  jars,  the  vitality  is 
retained  for  from  5  to  8  days.  In  bits  of  animal  tissue  containing  the 
bacilli,  the  vitality  is  retained  for  from  20  to  40  days,  according  to  the 
quantity  of  tissue  taken. 

Pathogenesis. — Subcutaneous  injections  of  from  i  to  3  c.  c.  rarely 
produce  fatal  results  in  swine.  An  intravenous  inoculation  of  5  c.  c. 
usually  produces  a  septicaemia.  With  smaller  doses  the  "button 
ulcers,"  characteristic  of  hog  cholera,  have  been  produced  (Welch). 
By  feeding  pigs  with  pure  bouillon  cultures  the  intestinal  lesions,  typical 
of  hog  cholera,  have  also  been  obtained  (Smith). 

Rabbits  inoculated  subcutaneously  with  o.  i  c.  c.  of  a  bouillon  cul- 
ture die  in  from  5  to  8  days.     The  essential  lesions  consist  of  necrotic 


174  HOG    CHOLERA 

foci  in  the  liver  and  a  very  much  enlarged  and  dark-colored  spleen. 
Guinea-pigs  are  affected  similarly  to  rabbits,  but  death  does  not  usually 
occur  until  from  7  to  12  days.  Pure  cultures  of  the  bacillus  can  be 
obtained  from  the  blood,  liver  or  spleen  of  the  inoculated  animals. 

While  the  above  description  applies  to  the  form  most  frequently 
encountered,  varieties  are  not  uncommon.  In  1894  Smith  called  atten- 
tion to  several  varieties  of  this  species.  It  is  interesting  to  add,  that 
Reed  and  Carroll  have  found  the  bacillus  isolated  by  Sanarelli,  and 
thought  by  him  to  be  the  cause  of  yellow  fever,  to  belong  to  this  group  of 
bacteria. 

§  136.  Symptoms.  The  sjaiiptoms  of  hog  cholera  are 
by  no  means  constant.  The  best  informed  writers  on  the  sub- 
ject agree  that  hog  cholera  can  not,  with  certain  exceptions,  be 
positively  diagnosed  from  the  symptoms.  Animals  suffering 
from  various  intestinal  troubles  frequently  exhibit  symptoms 
which  ver}'  closeh'  resemble  those  of  this  disease. 

There  are  two  recognizable  forms,  namely,  the  acute  and 
the  chronic  or  mild  form.  In  the  acute  disease,  the  animals 
die  very  suddenly  after  a  few  hours  or  at  most  a  few  days' 
sickness.  In  the  other  form,  the  disease  runs  a  longer  course. 
There  is  usually  a  rise  of  temperature  of  from  i  to  3°  F. 

The  sick  animals  act  dumpish,  spiritless  and  lie  quietly 
in  a  corner  or  huddle  together  usually  concealing  the  head  in 
the  litter.  They  refuse  to  move  when  disturbed  and  are  more 
or  less  oblivious  to  their  suffering.  The  appetite  varies.  In 
acute  cases  the  animals  may  eat  quite  heartily  up  to  within  a 
few  hours  before  death.  In  more  chronic  forms  they  eat  fairly 
well  until  the  end.  There  may  or  may  not  be  diarrhoea.  Fre- 
quently the  bowels  are  costive.  It  is  quite  common  in  these 
cases  to  have  an  active  diarrhoea  during  the  last  few  da3'S.  The 
color  of  the  discharge  depends  largely  on  the  food.  \'omiting 
rarely  occurs.  The  changes  in  the  respiration  and  the  pulse 
are  difficult  to  determine.  There  is  rarely  any  cough.  Usually 
there  is  considerable  reddening  of  the  skin  on  the  nose,  ears, 
abdomen  and  on  the  inside  of  the  thighs  and  pubic  region. 
Occasionally  this  reddening  is  very  marked.  The  redness  is 
diffuse  and  more  intense  as  death  approaches.  In  some  cases 
there  is  a  discharge  from  the  eyes.  In  the  chronic  form  the 
animal  becomes  emaciated.  These  symptoms  vary  to  such  an 
extent  that  it   is  sometimes  necessary  to  make  a  post-mortem 


MORBID    ANATOMY  I  75 

examination  and  even  then  the  diagnosis  must  often  be  delayed 
until  the  results  of  a  bacteriological  examination  have  been 
obtained.  It  not  infrequentl}^  happens  that  swine  suffering 
from  hog  cholera  are  attacked  with  swine  plague,  the  two 
diseases  co-existing  in  the  same  animal. 

§  137.  Morbid  anatomy,  (a)  The  acute  type.  This 
might  with  equal  propriety  be  called  the  hemorrhagic  or  sep- 
ticaemia type,  inasmuch  as  the  chief  and  perhaps  the  only 
obvious  changes  are  hemorrhagic  in  nature.  They  are  more 
conspicuous  when  an  animal  is  examined  immediately  after 
death.  The  spleen  is  variably  enlarged,  soft,  and  gorged  with 
blood.  Sometimes  it  is  twice  as  long  as  the  normal  spleen 
and  the  other  dimensions  being  proportionately  increased  it 
may  extend  across  the  median  line  to  the  right  side.  Next  to 
the  spleen,  the  lymphatic  glands  and  serous  membranes  are 
most  severel}^  involved.  The  cortex  of  the  glands  appears  on 
section  as  a  hemorrhagic  line  or  band,  according  to  the  amount 
of  extravasated  blood,  or  the  entire  gland  may  be  infiltrated 
with  it.  Among  the  glands  most  commonly  hemorrhagic  are 
those  of  the  meso-colon,  those  at  the  root  of  the  lungs,  and  on 
the  posterior  thoracic  aorta.  Besides  these,  the  retro-perito- 
neal and  the  gastric  glands  may  be  involved.  More  rarely  the 
mesenteric  glands  show  slight  blood  extravasations.  Hemor- 
rhages are  also  quite  frequent  beneath  the  serous  surfaces  of 
the  abdomen  and  thorax.  They  are  most  abundant  as  pete- 
chiae  and  larger  patches  under  the  mucous  membrane  of  the 
large  and  small  intestines.  They  are  occasionally  found  under 
the  peritoneum  near  the  kidneys,  the  diaphragm  and  the  costal 
pleura  as  extravasations  nearly  an  inch  in  diameter. 

The  lungs,  in  a  small  percentage  of  cases,  show  subpleural 
ecchymoses  in  large  numbers  and  on  section  small  hemor- 
rhagic foci  are  observed  throughout  the  lung  tissue.  In  a  few 
cases  severe  hemorrhages  involving  one  or  more  lobes  have 
been  observed.  The  kidneys  are  occasionly  the  seat  of  extensive 
hemorrhagic  changes.  The  glomeruli  appear  as  blood  red 
points  ;  larger  extravasations  occur  in  the  medullary  substance 
and  blood  may  collect  around  the  apices  of  the  papillae.  The  sub- 
cutaneous tissue  over  the  ventral  surface  of  the  body  ma}'  be 


176 


HOG    CHOLERA 


dotted  with  petechiae  and  occasionally 
collections  of  blood  (heniatomata)  are 
found  in  the  superficial  muscular  tis- 
sue. The  brain  and  spinal  cord  have 
not  been  generally  examined.  In  one 
case,  petechiae  were  observed  on  the 
cerebellum. 

The  digestive  tract  usually  is  the 
seat  of  extensive  lesions.  The  fundus 
of  the  stomach  is  as  a  rule  deeply  red- 
dened ;  there  may  be  more  or  less 
hemorrhage  on  the  surface,  giving 
rise  to  patches  or  larger  areas  of  blood 
clots.  In  some  cases  the  small  in- 
testine has  submucous  ecchynioses 
throughout  its  entire  length.  In  the 
large  intestine  these  ma}'  be  so  numer- 
ous as  to  give  the  membrane  a  dark 
red  appearance.  The  intestinal  con- 
tents are  now  and  then  found  incased 
in  a  layer  of  blood  clot. 

{b)  The  chronic  form  is  perhaps 
the  most  common,  at  least  in  those 
epizootics  which  have  been  reported. 
The  acute  hemorrhagic  cases  usually 
die  in  the  beginning  of  an  outbreak 
and  are  apt  to  be  overlooked.  Follow- 
ing these  are  the  more  protracted  ones. 
In  these  animals  the  disease  may  be 
limited  in  its  manifestations  to  the 
intestine  of  a  pig  dead  of  large  intestine  although  the  other  or- 
hog  cholera.  gans  are  not  exempt  from  degenerative 

changes.  These  are  due  in  part  to  the  impairment  of  the  func- 
tions of  the  large  intestine,  consequent  fermentations  and  the 
absorption  of  the  poisonous  products  elaborated  by  the  spe- 
cific bacilli  in  the  spleen  and  other  organs. 

The  lesions  of  the  large  intestines  are  necrotic  and  ulcera- 
tive in  character.     The  ulcers  may  be  isolated  and  appear  as 


Fig.  40.      Ulcers  in  the 


MORBID    ANATOMY 


177 


circular,  slightly  projecting 
masses,  stained  yellowish  or 
blackish  or  both  in  alternate 
rings,  or  they  may  be  slighth' 
depressed  and  somewhat  ragged 
in  outline.  When  the  superficial 
slough  is  scraped  away  many  ul- 
cers show  a  grayish  or  white  base. 
A  vertical  section  reveals  a 
rather  firm  neoplastic  growth, 
extending  usually  to  the  inner 
nuiscularcoat.  When  sections  of 
such  an  ulcer  are  stained  with 
aniline  dyes  and  examined  under 
the  microscope,  the  submucous 
tissue  is  very  much  thickened, 
infiltrated  with  round  cells  and 
containing  a  large  number  of  di- 
lated vessels.  Resting  upon  this 
thickened  subnuicosa,  is  a  line  of 
very  deeply  stained  amorphous 
matter  and  upon  this  is  situated 
the  necrotic  mass  which  fails  to 
retain  the  coloring  matter  and 
which  is  permeated  by  an  im- 
mense number  of  bacteria  of  vari- 
ous kinds.  Frequently  the  eggs 
of  trichocephalus  are  imbedded 
in  the  slough. 


Spleens  of  pigs  of 
[a]  dead  from  hog 


Fig.  41. 
The  extent    of    the  submu-   the  same  age 

cous  infiltration  depends  upon  cholera;  [b)  normal,  {killed  iti 
the    age   of   the  ulcer.      In    old   ^"'<'^^^n- 

ulcers  it  contains  many  newdy-formed  capillaries  and  evidences 
of  the  formation  of  connective  tissue  are  present.  The  capil- 
laries may  extend  to  the  very  edge  of  the  border  where  the 
slough  begins.  The  latter  may  have  been  partly  shed,  leaving  a 
smooth  line  bounding  the  cicatricial  tissue.  The  submucous  in- 
filtration gradually  disappears  toward  the  periphery  of  the  ulcer 


I 78  HOG    CHOLERA 

and  slightly  outside  of  the  ulcer  no  inflammation  of  the  mem- 
brane exists.  Giant  cells  have  been  observ'ed  in  the  intertubular 
tissues  at  the  edge  of  the  ulcer.  The  depth  to  which  the  infiltra- 
tion extends  is  not  always  limited  to  the  submucosa  ;  it  may 
extend  into  the  muscular  coats  and  cause  inflammatory  thick- 
ening and  inflammation  and  the  formation  of  new  vessels  in 
the  subjacent  serosa. 

In  some  cases  the  necrosis,  instead  of  appearing  in  circum- 
scribed ulcers  from  one-sixteenth  to  one-half  inch  or  more 
across,  involves  the  whole  surface  of  the  mucous  membrane, 
giving  it  the  appearance  of  a  so-called  diphtheritic  membrane. 
In  such  cases  the  walls  of  the  intestine  are  very  much  thick- 
ened and  so  friable  as  to  be  easily  torn  wath  the  forceps  in 
handling  them.  Such  necroses  are  rare  in  epizootic  cases,  but 
it  frequently  appears  in  animals  which  have  been  fed  with 
pure  cultures  of  hog  cholera  bacilli. 

The  distribution  of  the  ulcers  varies  but  slightly.  They 
appear  most  frequently  in  the  caecum  and  on  the  ileo-caecal 
valve,  as  well  as  in  the  upper  half  of  the  colon.  The  lower 
half  is  implicated  in  severe  cases  only  and  then  less  ex- 
tensiveh-.  The  rectum  is  rarely  ulcerated.  The  lower  por- 
tion of  the  ileum  is  ulcerated  in  a  small  percentage  of  animals, 
especially  when  they  have  been  fed  with  hog  cholera  vis- 
cera or  cultures.  The  stomach  is  occasionally  the  seat  of 
slight  ulceration.  The  lymphatic  glands  of  the  affected 
intestine  are  usually  much  enlarged,  pale,  tough  and  whitish 
on  section.  The  spleen  is  rarely  enlarged  ;  the  liver  shows 
degenerative  changes.  The  heart  and  lungs  are  usually  normal. 
The  broncho-pneumonia  frequently  found  in  young  pigs  in  the 
winter  months  must  be  ascribed  primarily  to  exposure  rather 
than  to  the  presence  of  hog  cholera. 

In  some  outbreaks  the  acute  and  the  chronic  types  of  the 
disease  are  not  so  clearly  separated  as  given  in  the  foregoing 
pages.  Frequentlj^  recent  hemorrhagic  lesions  seem  to  be 
associated  with  cases  presenting  extensive  ulcerations,  which 
certainly  are  much  older  than  the  extravasations.  It  may  be 
that  the  latter  are  the  result  of  a  secondary  invasion  of  the 
hog-cholera  virus,  either  from   the  ulcers   in  the  intestine  or 


MORBID    ANATOMY  I  79 

from  without.  To  illustrate  more  fully  the  differences  in  the 
lesions  of  the  two  forms  of  the  disease,  the  published  post- 
mortem notes  of  two  cases  are  appended. 

(i)  Acute  form.  Female,  two  years  old,  weight  about  250  pounds. 
She  had  been  known  to  be  sick  but  a  few  hours.  The  examination  was 
made  two  hours  after  death.  A  littte  blood  was  oozing  from  the  nostrils. 
The  skin  was  not  discolored.  Upon  section  the  flesh  was  normal  in 
appearance.  The  liver  was  deeply  reddened  due  to  engorgement  of  the 
blood  vessels.  Blood  flowed  freely  upon  section.  The  spleen  was 
slightly  enlarged  and  dark  colored.  The  kidneys  were  hyperaemic, 
especially  the  mc-dullary  portion.  In  the  pelvis  of  the  right  kidney 
there  was  a  large  blood  clot.  The  mucous  membrane  of  the  intestines 
was  normal  with  the  exception  of  several  irregular  areas  of  hyperaemia. 
In  the  fundus  of  the  stomach  was  a  large,  dark  blood-clot.  No  ulcers. 
The  mesenteric  glands  were  enlarged  and  darker  than  normal.  In  a  few 
cases  the  cortex  was  hemorrhagic.  The  right  lung  was  in  a  state  of 
hyperaemia.     The  heart  contained  very  little  liquid  blood. 

Bacteriological  exiDuination. — A  few  bacteria  were  found  in  stained 
cover-glass  preparations  from  the  spleen  and  liver.  Tubes  of  slant 
agar  were  inoculated  with  bits  of  the  tissue  from  the  hyperaemic  lung, 
liver,  spleen  and  kidneys.  These  tubes  developed  cultures  of  the  hog- 
cholera  bacillus.  A  few  of  them  were  pure  cultures;  the  others  con- 
tained, in  addition  to  the  hog- cholera  organism,  a  quite  large  bacillus. 
(Report  N.  Y.  State  Com.  Agric.  1887) 

(2)  Chro7iic form.  Small  female,  weight  about  50  lbs.  Considerable 
reddening  of  the  skin  over  the  ventral  aspect  of  the  body  and  limbs  ; 
especially  marked  along  the  median  line.  Superficial  inguinals  enlarged, 
of  a  mottled,  pale  and  deep  red  on  section.  Spleen  very  large,  12  inches 
long,  2  inches  broad,  and  five-eighths  to  three  fourths  inches  thick  at 
the  hilus  ;  gorged  with  blood,  friable.  A  small  number  of  punctiform 
hemorrhages  in  cortical  portion  of  the  kidneys.  Glands  of  mesentery 
and  colon  enlarged  and  congested.  Deep  reddening  of  several  square 
inches  of  mucosa  in  fundus  of  stomach.  Large  intestine  contains  a  semi- 
liquid  mass  chiefly  earth.  Four  large  ulcers  in  the  caecum,  one  of  them 
at  least  one  inch  across,  covered  by  a  yellowish  slough  ;  the  peritoneum 
covering  it  is  thickened  and  inflamed.  In  upper  colon  there  is  consider- 
able necrosis,  involving  the  epithelium  in  patches.  Lungs  normal, 
excepting  the  right  ventral  lobe,  which  is  solid.  Bronchi  and  air  cells  of 
this  lobe  completely  occluded  by  plugs  ;  surface  bright  red,  mottled  with 
yellowish  points — the  ultimate  air  cells  filled  with  the  cellular  exudate. 
Subpleural  ecchymoses  over  both  lungs.  From  the  spleen  a  liquid  and 
a  gelatin  culture  contained  only  hog  cholera  bacteria.  They  were  verj- 
numerous  in  cover-glass  preparations  from  this  organ. 

A  rabbit  inoculated  from   the  consolidated  lung  tissue  died  on  the 


l8o  HOG    CHOLERA 

seventh  da}'.  At  the  point  of  inoculation  a  pasty  mass  extends  to  abdo- 
men, only  subcutis  involved.  Spleen  engorged.  Single  acini  in  the  liver 
are  completely  necrosed,  yellowish  white.  In  both  organs,  hog  cholera 
bacteria.     Cultures  from  spleen  pure.    (Report  on  hog  cholera,  1S89. ) 

§  138.  Differential  diagnosis.  Hog  cholera  is  to  be 
differentiated  from  a  great  variety  of  dietary  disorders  and 
poisoning  from  alkalies  and  possibly  from  other  chemicals 
which  may  get  into  their  food.  Powdered  soap  has  been  found 
to  produce,  when  given  in  sufficient  quantities,  a  series  of 
symptoms  quite  similar  to  those  of  hog  cholera.  In  addition 
to  the  many  as  yet  etiologically  undetermined  disorders  often 
giving  a  high  mortality  and  popularly  called  hog  cholera,  infec- 
tious pneumonia  or  swine  plague  and  tuberculosis  are  to  be 
distinguished  from  it. 

It  sometimes  happens  that  swine  when  kept  under  good 
hygienic  conditions  suffer  from  disorders  which  in  their  symp- 
toms resemble  hog  cholera,  but  anatomically  the  lesions  are 
varied  and  irregular.  A  few  such  enzootics  have  been  studied. 
A  few  have  been  described.  In  one  instance  B.  coli  com- 
munis seemed  to  stand  in  a  casual  relation  to  the  trouble. 
Recently  the  writer  has  studied  two  similar  enzootics  where 
several  animals  died  and  where  the  lesions  were  very  few 
and  exceedingly  varied.  In  some  of  them  there  were  healing, 
intestinal  ulcers  and  the  bacillus  isolated  belonged  to  the  para- 
colon group.  It  may  be  supposed  that  possibly  many  of  these 
mild  cases  (enzootics)  are  modified  hog  cholera.  At  present, 
however,  stich  a  conclusion  does  not  seem  to  be  fully  justified. 

The  dietary  disorders  are  excluded  from  the  history,  the 
irregularity  of  the  lesions  and  the  failure  to  find  the  specific 
organism  of  hog  cholera  in  the  tissues  of  the  dead  animals. 
An  important  feature  is  the  fact  that  the  trouble  docs  not 
extend  beyond  the  herd  or  herds  first  attacked  or  animals  fed 
and  kept  under  like  conditions. 

In  differentiating  hog  cholera  from  swine  plague  much  de- 
pends upon  the  specific  bacteria.  While  in  typical  chronic  cases, 
the  intestinal  lesions  in  hog  cholera  and  the  lung  affections  in 
swine  plague  are  sufficient,  in  many  cases  and  outbreaks  the 
variations  of  the    lesions    are  such    that  diagnosis   must  de- 


DIFFERENTIAL    DIAGNOSIS 


l8l 


pend  upon  the  bacteriological 
ences  between  the  two  species 
the  comparison  appended. 

Bacillus  of  hog  cholera. 

1.  Rod-shaped  organism  with 
ends  rounded,  1.2  to  2.011  in  length, 
0.5  to  0.8.'  in  width.  The  size  varies 
according  to  the  stage  of  growth 
and  division  and  the  culture  media. 

2.  From  cultures  it  stains  en- 
tirely. In  tissues  it  usuall}- stains 
around  the  periphery  leaving  a 
light  centre. 


3.  Actively  motile  in  liquids. 

4.  From  3  to  9  flagella  are  de- 
monstrable. 

5.  Vigorous  growth  in  alkaline 
nutrient  liquids.  Less  vigorous  if 
liquids  are  acid  in  reaction. 

6.  Moderate  growth  on  potato. 
(Varies  according  to  reaction.  ) 

7.  Distinct  growth  on  gelatin. 

8  Saponiiiesmilk  in  from  3  to  4 
weeks. 

9.  Ferments  de.xtrose  with  the 
formation  of  acids  and  gas. 

10.  Does  not  ferment  lactose. 
Bouillon  containing  it  becomes 
strongly  alkaline.     No  gas. 

11.  Does  not  ferment  saccha- 
rose Bouillon  containing  it  be- 
comes strongly  alkaline      No  gas. 

12.  Destroyed  by  moist  heat  at 
58°  C.  in  15  minutes. 

13.  Dies  in  water  in  from  2  to  4 
months. 

14.  It  dies  in  the  soil  in  from  2 
to  3  months. 

15.  Rabbits  injected  subcutane- 
ously  with  o.i  c.c.  of  a  bouillon 
culture  of  a  virulent  bacillus  will 
die  in  from  5  to  7  days.  Enlarged 
spleen,  necrotic  foci  in  liver. 


findings.     The  essential  differ- 
of  bacteria   are  brought  out  in 

Bacterium  of  swine  plague. 

1.  Enlongated  oval  organism 
0.8  to  1.5//  in  length,  0.6  to  o  8//  in 
thickness.  The  size  varies  accord- 
ing to  the  stage  of  growth  and 
division  and  the  culture  media. 

2.  From  old  cultures  it  usually 
stains  entirely.  When  in  pro- 
cess of  division  as  found  in  the 
organs  of  freshly  dead  rabbits  the 
extremities  stain  leaving  an  un- 
stained central  band,  "polar  stain." 

3.  Not  motile  in  liquids. 

4.  No  ilagella  have  been  found. 

5.  Growth  moderate  or  feeble 
in  alkaline  nutrient  liquids.  No 
growth  if  liquids  are  acid. 

6.  No  growth  on  potato. 


7.  Feeble  or  no  growth  on  gela- 
tin. 

8.  Produces  no  apparent  change 
in  milk. 

9.  Ferments'dextrose  with  the 
formation  of  acids  but  no  gas. 

10.  Does  not  ferment  lactose. 
No.  gas. 

11.  Ferments  saccharose  with 
the  formation  of  acids.      No.  gas. 

12.  Destroyed  by  moist  heat  at 
58°  C.  in  7  minutes. 

13.  Dies  in  water  in  from  10  to 
15  days. 

14.  It  dies  in  the  soil  in  from  4 
to  6  days. 

15.  Rabbits  injected  subcutane- 
ously  with  o.oi  c.c.  of  a  bouillon 
culture  of  a  virulent  bacillus  will 
die  in  from  16  to  20  hours.  Septi- 
caemia. 


I82 


HOG    CHOLERA 


i6.  Rabbits  inoculated  with  cul- 
ture of  an  attenuated  variety  live 
from  lo  to  20  days  or  recover. 
The  lesions  are  enlarged  spleen, 
and  infiltration  of  the  follicles  in 
Peyer's  patches. 

17.  In  guinea-pigs  the  lesions 
are  practically  the  same  as  in  rab- 
bits. Death  occurs  in  from  7  to  12 
days. 

18.  Pigs  are  not  usually 
affected  by  subcutaneous  injection 
of  small  quantities  of  culture.  If 
the  pigs  are  killed  within  i  to  3 
weeks  the  bacilli  are  found  in  the 
local  lesion  and  certain  of  the  lym- 
phatic glands.  Fatal  results  are 
reported  in  a  few  cases  by  these  in- 
jections. 

19.  Feeding  cultures  to  pigs 
which  have  fasted  for  24  hours 
produces  extensive  intestinal  lesi- 
ons with  fatal  results. 

20.  Intravenous  inoculation  in- 
to pigs  causes  either  an  acute  sep- 
ticaemia or  a  chronic  form  of  the 
disease  in  which  are  produced 
quite  typical  round,  firm,  elevated 
ulcers. 


16.  Rabbits  inoculated  with  a 
culture  of  an  attenuated  variety 
will  live  from  4  to  10  days.  The 
lesions  are  local  infiltration  of  pus 
cells  with  pleuritis,  pericarditis  or 
peritonitis. 

17.  Guinea-pigs  are  slightly 
less  susceptible  than  rabbits.  There 
is  more  local  reaction.  Death  oc- 
curs in  from  i  to  4  days. 

18.  Pigs  are  not  usually  affected 
by  the  subcutaneous  injection  of 
small  -quantities  of  culture.  The 
bacilli  are  not  found  except  in  the 
local  lesion.  In  a  few  cases  fatal 
results  are  reported. 


19.     Feeding    cultures    to     pigs 
usually  produces  no  effect. 


20.  Intravenous  inoculation  in- 
to pigs  usually  produces  a  septic 
form  of  the  disease  which  kills  in 
from  I  to  2  days.  Inoculation  into 
the  lungs  causes  pleuritis,  usually 
accompanied  by  pneumonia. 


§  139.  Prevention.  As  hog  cholera  is  caused  by  a 
specific  organism  the  first  fact  to  be  determined  is  to  find  the 
channel  or  means  b}'  which  it  can  be  carried  from  an  infected 
to  a  |non-infected  herd.  The  thorough  investigations  which 
have  been  made  in  the  United  States  Bureau  of  Animal  Indus- 
try have  shed  much  light  upon  this  subject.  The  observa- 
tions of  more  recent  years  have  confirmed  the  conclusion 
reached  in  the  earlier  reports  of  the  Bureau  concerning  the 
means  of  spreading  this  disease.  With  these  results,  the 
pointing  out  of  the  ways  by  which  the  virus  may  be  dissemin- 
ated and  the  methods  necessar}"  for  checking  its  .spread  is  no 
longer  questionable  and  there  is  a  certainty  that  it  can  be  kept 
away  from  individual  herds  even  in  the  midst  of  wide  spread 


PREVENTION  1 83 

epizootics.      A  few  of  the  common  means  of  its  dissemination 
are  worthy  of  note. 

1 .  The  virus  of  hog  cholera  is  frequently  introduced  into 
a  non-infected  locality  by  the  purchase  of  animals,  usually  for 
breeding  purposes,  from  herds  in  which  this  disease  exists  or 
has  existed  within  the  preceding  few  months.  These  animals 
are  usually  placed  among  the  home  raised  swine  without 
quarantine  thus  affording  every  possible  facility  for  starting 
up  a  new  outbreak.     The  reason  for  this  is  clear. 

The  bacteria  can  be  carried  in  the  dirt  on  the  animals 
or,  as  is  most  usually  the  case,  the  pigs  may  have  been  but 
recently  infected  and  being  transferred  during  the  period  ot 
incubation  they  develop  the  disease  later.  It  not  infrequently 
happens  that  the  purchased  animals  are  actually  suffering 
from  a  chronic  form  of  the  disease,  to  which  they  eventually 
succumb  but  meantime  infecting  others.  In  purchasing  swine, 
therefore,  it  is  of  the  greatest  importance  that  the  history  of 
the  herd  should  show  that  it  had  been  free  from  infectious 
diseases  for  at  least  one  year.  In  addition  to  this,  newly 
purchased  swine  should  not  be  placed  immediately  after  ship- 
ment in  the  pens  with  the  home  stock,  but  they  should  be  kept 
in  a  separate  enclosure  until  all  danger  of  the  disease  has 
passed. 

2.  Swine  are  often  shipped  in  crates,  boxes  or  in  open 
cars  in  which  hogs  affected  with  hog  cholera  have  previously 
been  confined.  The  history  of  hog  cholera  contains  many 
illustrations  of  this  method  of  contracting  the  disease. 

3.  The  bacilli  of  hog  cholera  live  for  a  considerable  time  in 
water.  On  this  account  the  bacteria  from  outbreaks  which  start 
at  or  near  the  source  of  a  creek  or  small  river  may  be  carried 
in  the  current  and  infect  animals  which  wallow  in  the  stream 
many  miles  below.  By  keeping  swine  in  a  small  enclosure 
away  from  infected  streams  and  fields  the  disease  is  often 
prevented. 

4.  The  bacilli  of  hog  cholera  can  be  carried  in  the  dirt 
which  adheres  to  one's  shoes  or  to  farming  utensils.  It  not 
infrequently  happens  that  the  virus  of  this  disease  is  carried 
from  farm  to  farm  on  the  tools   taken   from   an  infected  place. 


184  HOG    CHOI.ERA 

5.  The  virus  ma}-  be  carried  b}-  buzzards,  crows  and 
other  birds.  There  is  no  positive  proof  that  the  virus  has  been 
disseminated  in  this  way  although  there  is  much  evidence  to 
support  such  a  theory,  particularly  in  the  South.  Several  out- 
breaks have  been  attributed  to  this  method  of  introducing  the 
virus.  The  hypothesis  emphasizes  the  necessity  for  prompth^ 
disposing  of  the  dead  animals  instead  of  leaving  them  as  prey 
for  scavengers.  If  the}'  cannot  be  burned  it  is  best  to  cover 
the  bodies  with  a  liberal  amount  of  lime  and  bury  them. 

§  140.  Specific  treatment.  A  large  number  of  inves- 
tigations have  been  made  to  find  a  protective  vaccine  method 
for  this  disease  and  also  to  find  a  specific  serum  treatment. 
Thus  far  satisfactory  experimental  results  have  not  been 
obtained.  In  a  number  of  instances  where  the  practical 
applications  of  the  "serum  treatment"  has  been  made,  most 
satisfactory  results  followed,  but  the  reports  fail  to  give  evi- 
dence of  an  accurate  diagnosis  of  the  disease  treated.  In 
these  cases,  the  better  management  of  the  animals,  in  addition 
to  the  serum,  would  suffice  to  check  the  disease  if  the  trouble 
was  of  a  dietary  nature.  There  is  need  for  additional  inves- 
tigation along  these  lines. 

REFERENCES. 

1.  Billings.  Bidletins  Neb.  Agric.  Expt.  Staiiott  1888.  Also  many 
special  publications  ajid  contributions  to  various  veterinary  journals. 

2.  Dawson  The  serum  diagnosis  of  hog  cholera.  New  York  3/cd. 
four.  Feb.  20.  iSgj. 

3.  DE  SCHWEiNiTz.  The  production  of  inmuinitj'  in  guinea  pigs 
from  hcg  cholera  by  :he  use  of  blood  serum  from  iir.ii;uniz"d  animals. 
Annual  Report  of  the  Bureau  of  Animal  Industry,  U.  S.  Dept.  of  Agri- 
culture. i8gS. 

4.  Peters.  Serum  therapy  in  hcg  cholera.  Bulletin  No.  4J. 
Univ.  of  Neb.  Agri.  Exper.  Station.     iSgy. 

5.  Salmon  and  Smith.  Annual  Reports  of  the  Bureau  of  Ani- 
mal Industry.     iSS^-i8g^. 

6.  Salmon.  vSpecial  Report  on  hog  cholera,  its  History,  Nature 
and  Treatment.      U.  S.  Bureau  of  Animal  Industry.     1SS9. 

7.  Smith.     Zur  Kenntniss  des   Hog  cholera  Bacillus.     Antralhlatt 
fur  Bakler.     u.  Parasitenkunde.     Bd.  IX.    (1S91)  S.  253. 

8.  Smith.  Hog  cholera  group  of  bacteria.  Bulletin  No.  6  U.  S. 
Bureau  of  Animal  Industry.     1894.  p.  9. 

9.  Smith  and  Moore.  Experiments  on  the  production  of  immu- 
nity in  rabbits  and  guinea  pigs  v.ilh  reference  lo  hog  cholera  and  swine 
plague  bacteria.     Ibid.  p.  41. 


TETANUS  185 

10.  Reed  and  Carroll.  Bacillus  \cteroi'\e&  and  Bacilltis  cko/erae 
suis.     A  preliminary  note.      T/ie  Medical  News.     Apr.  2g,  iSgg 

11.  Welch  Report  of  investigations  concerning  the  causation 
of  hog  cholera.    Johns  Hopkins  Hospital  Bulletin.     No.  i.     18S9. 

12.  Welch  and  Clements.  Remarks  on  hog  cholera  and  swine 
plague.  First  International  Congress  of  America  held  in  Chicago,  111., 
October,  1893. 


TETANUS. 


§141.  Characterization.  Tetanus  is  an  infectious  dis- 
ease (toxaemia)  in  which  specific  organism  is  localized  at  the 
place  of  inoculation.  It  is  characterized  by  spasmodic  con- 
traction of  the  muscles,  referable  to  the  nervous  system  and 
by  the  absence  of  obvious  tissue  changes.  It  is  the  result  of 
a  specific  wound  infection.  All  mammalia  including  man  are 
susceptible.  It  occurs  most  frequently  in  horses,  asses  and 
mules  ;  next  to  them  in  the  smaller  ruminants  such  as  the 
sheep  and  goat  ;  it  appears  least  often  in  the  dog.  It  is 
reported  to  occur  rarely  in  birds  and  fowls  are  supposed  to  be 
immune.     The  human  species  is  very  susceptible. 

§  142.  History.  Tetanus  is  one  of  the  diseases  that 
was  recognized  and  described  before  the  Christian  era.  It 
was  not  clearly  differentiated  until  the  discovery  of  its  specific 
cause  in  1884. 

Ji  143.  Geographical  distribution.  Tetanus  is  reported 
to  be  more  prevalent  in  the  hot  climates  than  in  the  temperate 
ones,  while  in  the  very  cold  latitudes  it  is  rarely  if  ever 
encountered.  It  is  more  frequently  met  with  in  some  districts 
than  in  others.  Although  very  common  in  certain  localities, 
it  is,  on  the  whole,  a  somewhat  rare  disease.  There  seems  to 
be  no  statistics  by  which  its  frequency  can  be  determined 
in  this  country,  but  in  certain  of  the  European  armies  this 
has  been  noted.  In  the  Prussian  army,  it  is  reported  to 
occur  once  in  a  thousand  cases  of  sickness  among  horses.  At 
Wlirttemberg,  Hering  reports  it  once  in  3000  cases  of  disea.se 
among  the  horses  in  the  cavalry.  It  has  also  been  noted  that 
in  some  veterinary  hospitals  it  does  not  occur  for  long  periods, 
while  at  other  times  several  cases  may  appear  in  rapid  succession. 
It  is,  however,  a  wide  spread  disease. 


I 86  TETANUS 

§  144.     Etiology.     Tetanus  is  caused 
by  a  slender  bacillus  2  to  5/<  in  length.      It  1^^^ 

forms  spores  which  are  at  the  end  of  the  or-  ^\        V 

ganism  giving  it  somewhat  the  appearance         \  f   ^^ 

of  a  pin.      On  account  of  this  it  has  been  \    '    ^ 

designated    the  "pin    bacillus."      It    is  an-       •^"'^  ^ 

aerobic.  This  organism  was  first  observed  Fig.  42.  Bacillus 
by  Nicolaier  in  1885,  although  Carle  and  ^^^'""' 
Rattone  showed  in  1884,  that  this  disease  could  be  transmitted 
from  man  to  animals  by  inoculation  with  the  pus  from  the  local 
lesion.  In  1889,  Kitasato  isolated  the  bacillus  and  studied  it 
in  pure  culture.  This  bacillus  stains  readily  with  the  aniline 
dyes,  especially  with  carbol-fuchsin.  It  takes  the  Gram  stain. 
It  grows  well  in  nutrient  gelatin,  agar  or  bouillon  and  on  blood 
serum  at  the  temperature  of  the  body  and  in  an  atmosphere  of 
hydrogen  or  in  the  absence  of  air  as  in  deep  agar  cultures.  The 
addition  of  a  little  grape  sugar  facilitates  its  growth.  It  has 
the  di.stinction  of  producing  the  most  powerful  (poisonous?) 
toxinof  any  known  bacteria,  0.23  of  a  milligram  being  estimated 
as  a  fatal  dose  for  a  man  of  175  pounds  weight. 

The  fact  that  this  bacillus  is  an  anaerobe  renders  its  culti- 
vation of  little  practical  value  in  diagnosing  the  disease.  Al- 
though it  is  not  distributed  in  the  body,  it  can  usually  be  found 
in  cover-glass  preparations  made  from  the  local  lesion  and 
stained  with  carbol  fuchsin. 

Bacillus  tetaiii  is  found  in  the  soil.  It  has  been  found  in 
hay  dust,  in  the  mortar  of  old  masonry,  in  the  dust  in  rooms, 
barracks  and  hospitals  and  in  the  arrow  poison  of  certain  savages 
in  the  New  Hebrides.  They  obtain  it  by  smearing  their  arrow 
heads  with  mud  from  crab  holes  in  the  swamp.  It  is  reported 
that  certain  savages  in  Africa  destroy  their  enemies  by  putting 
bits  of  broken  glass  mixed  with  certain  soils  in  their  shoes. 
The  cause  of  death  is  tetanus.  Mould  rich  in  horse  manure 
seems  to  be  the  most  favorable  abode  for  it.  It  has  been 
stated  that  it  exists  in  all  soils.  There  are  good  reasons  for 
believing  that  this  is  an  over  estimate  of  the  wideness  of  its 
distribution.  It  certainly  is  more  numerous  in  some  localities 
than  in  others. 


MODE    OF    INFECTION  1 87 

The  tetanus  bacillus  is  very  resistant,  especially  in  its 
spore  form,  to  destructive  agents  such  as  drying  and  the  or- 
dinary disinfectants.  Kitasato  found  that  a  5  per  cent  sol ution_ 
of  carbolic  acid  applied  for  ten  hours  failed  to  kill  the  spores^, , 
Tizzoni  and  Cattani  found  that  mineral  and  organic  acids  pro- 
duced no  effect  upon  the  dried  spores.  Behring  found  that 
iodine  trichloride  possesses  a  strong  antiseptic  effect  upon  them. 
They  are  not  affected  by  the  gastric  fluids.  It  has  been  noted 
by  Kitt  that  the  dried  spores  in  pus  have  retained  their  viru- 
lence for  sixteen  months.  They  are  destroyed  when  subjected 
to  a  temperature  of  100°  C.  in  water  or  steam  for  ten  minutes. 
The  bacilli  in  the  vegetative  state  are  readily  destroyed  by  the 
usual  strong  disinfectants,  such  as  5  per  cent  carbolic  acid. 

A  number  of  pseudo-tetanus  bacilli  have  been  described. 
This  renders  a  careful  study  of  the  suspected  organism  neces- 
sary as  it  is  difficult  in  some  cases  to  determine  microscopically 
B.  tetani.  The  guinea  pig  inoculation  affords  a  ready  m.eans 
of  differentiation  whenever  fresh  material  is  available. 

§  145.  Mode  of  infection.  As  the  bacillus  of  tetanus 
is  widely  distributed  in  the  soil  and  consequently  on  articles 
contaminated  with  it,  the  most  common  modes  of  infection  are 
punctures  scratches,  and  pricks  made  by  splinters,  nails  or 
infected  instruments  (traumatic  tetanus).  It  maj'  follow 
slight  abrasions  of  the  skin  where  infected  earth  comes  in  con- 
tact with  the  lacerated  epidermis.  Infection  through  wounds 
in  the  intestinal  mucosa  do  not  seem  to  have  been  clearly 
demonstrated.  The  most  usual  method  seems  to  be  by  pricks 
and  nail  punctures,  in  which  cases  the  virus  can  be  carried 
well  into  the  living  tissues  and  there  is  little  or  no  bleeding  to 
wash  it  out. 

Infection  often  occurs  in  young  foals  and  lambs  through 
the  freshly  broken  umbilical  cord  (tetanus  neonatorum). 
The  symptoms  begin  to  appear  in  a  variable  length  of  time 
after  the  infection  takes  place.  The  shortest  period  which 
seems  to  be  reported  is  a  few  hours  and  the  longest  is  six 
weeks.  In  horses  the  period  of  incubation  is  usually  from 
four  to  twenty  days.  After  inoculation  with  pure  cultures  it 
is  from  four  to  five  days  and  in  sheep  from  two  to  four  days. 


I 88  TETANUS 

In  guinea  pigs  inoculated  with  infected  soil  the  incubation 
period  is  usually  not  over  forty-eight  hours  and  often  less  than 
that.  Park  has  found  that  mice,  guinea  pigs,  rabbits,  rats, 
horses,  goats  and  a  few  other  animals  inoculated  with  pure  cul- 
ture have  a  period  of  incubation  of  from  one  to  three  days.  In 
man  it  varies  from  one  to  twenty  days.  There  are,  however,  a 
few  exceptionally  long  periods  reported.  It  has  been  noted  by 
Richter  and  others  that  the  shorter  the  period  of  incubation  the 
more  severe  the  disease,  the  mortality  being  over  90  per  cent  in 
the  first  and  about  50  per  cent  when  the  symptoms  were  slow 
in  appearing. 

§  146.  Symptoms.  The  first  symptoms  are  often 
obscure  and  ma}'  be  overlooked  for  several  days  or  they  may 
be  ushered  in  suddenly  with  violent  and  extensive  tonic  spasms. 
The  tetanic  spasms  usually  begin  in  the  muscles  of  the  head 
and  neck,  extending  from  these  to  the  muscles  of  the  throat, 
trunk  and  extremities.  It  often  happens  that  the  spasms  first 
appear  in  the  hind  quarters  and  extend  forward.  There  is 
stiffness  of  the  parts  affected.  If  in  the  head,  the  muscles  of 
mastication  are  first  attacked  with  spasms,  while  if  the  hind 
quarters  are  first  attacked,  there  are  usually  spasms  of  the 
muscles  of  the  tail.  The  muscles  at  the  site  of  inoculation  are 
frequently  the  first  to  show  spasms  and,  if  the  disease  is  of  a 
mild  type,  they  may  be  the  only  ones  to  exhibit  S3'mptoms. 
Friedberger  and  Frohner  have  grouped  the  muscles  which  are 
attacked  with  the  more  obvious  effects  upon  the  appearance 
of  the  animal.     They  are  as  follows,  viz.: 

(i).  The  muscles  of  mastication.  The  contraction  of 
these  muscles  is  called  trismus  or  "  lockjaw."  According  to 
the  degree  of  contraction  the  jaws  remain  in  more  or  less  close 
contact,  rendering  prehension  or  mastication  difficult  or  im- 
possible. 

(2).  The  other  muscles  of  the  head.  These  are  spasmodi- 
cally contracted  in  different  degrees.  Spasms  of  the  muscles 
of  the  ears  cause  the  ears  to  be  "  pricked  "  and  their  tips  to  be 
drawn  together  ;  of  the  recti  muscles  of  the  eyes,  cause  the 
eyes  to  be  retracted  in  the  orbit  with  protrusion  of  the  nictitat- 
ing membrane  ;  of  the  nose,  produce  dilatation  of  the  nostrils  ; 


SYMPTOMS  189 

of  the  dilator  of  the  upper  lip,  give  an  abnormal  shape  to  the 
opening  of  the  mouth.  The  muscles  of  the  tongue,  of  degluti- 
tion and  of  the  larynx  are  also  usually  attacked  by  spasms. 

(3).  The  extensor  muscles  of  the  neck.  Contraction  ol 
these  muscles  cause  a  stiff,  stretched  out  carriage  of  the  head 
and  "  ewe  neck."  The  muscles  of  the  neck  become  hard  and 
tense  to  the  touch. 

(4).  The  extensor  muscles  of  the  back.  Spasms  of  these 
muscles  are  manifested  by  an  extremely  hard  condition  of  the 
muscles  of  the  back,  loins  and  croup.  Several  conditions  may 
arise.  Orthotonvis  in  which  the  neck  is  stretched  out  and  the 
back  and  croup  are  carried  horizontally  or,  opisthotonus  in 
which  the  head  is  raised  and  drawn  back  and  the  vertebral 
column  slightly  depressed.  This  is  the  most  common  occur- 
rence. There  may  be  a  lateral  curvature  of  the  cervical 
vertebrae  which  is  uncommon  and  also  a  convex  curvature  of 
the  vertebrae  which  is  very  rarely  observed.  The  tail,  espe- 
cially in  horses,  is  often  raised  and  occasionally  said  to  be 
straight  with  the  back. 

(5J.  The  muscles  of  the  limbs.  The  spasms  in  these 
muscles  make  the  limbs  stiff  and  cause  the  animal  to  assume 
an  attitude  in  which  the  fore  legs  are  extended  forward  and 
laterally  and  the  hind  ones  backward  and  laterally.  They  are 
bent  at  the  joints  onh- with  difhculty.  The  contraction  of  the 
muscles  of  the  abdomen  gives  the  animal  a  tucked  up  appear- 
ance and  the  spasms  of  the  muscles  of  respiration  render 
breathing  difficult. 

Besides  the  spasms  the  animal  shows  an  increased  reflex 
irritability  and  heightened  sensibility.  These  manifest  them- 
selves in  excitement,  timidity  and  intensified  muscular  con- 
tractions if  irritated.  Sweating  is  common  especially  in  severe 
cases.  In  mild  cases  it  may  be  absent.  There  is  usually 
little  or  no  change  in  the  internal  temperature.  In  fatal  cases 
the  temperature  is  usualh'  constantly  high  toward  the  last. 
The  high  temperature  (104°  to  106°  F)  usually  continues  for 
some  time  after  death.  Bayer  has  observed  in  a  horse,  24 
hours  before  death,  a  temperature  of  102°  F  ;  one  and  a  half 
hours  before  death,  105°  F  ;  at  the  moment  of  death,  111°  F  ; 


I  go 


TETANUS 


and  fifty  minutes  after  death,  113°  F.  There  is  frequently  no 
increase  in  the  number  of  pulse  beats  until  severe  exacerba- 
tions set  in.  The  frequency  of  the  pulse  is  much  greater  in 
animals  which  continue  recumbent  than  in  those  which  keep 
upon  their  feet.  The  pulse  is  often  hard  and  small  and  the 
walls  of  the  arteries  are  spasmodically  tense.  In  many  cases 
however,  it  is  full,  soft  and  easily  compressible.  There  is,  as 
a  rule,  an  increase  in  the  number  of  respirations,  which  may 
become  very  high  if  the  respiratory  muscles  are  attacked. 
The  number  varies  according  to  the  excited  condition  of  the 
animal.  The  respirations  may  increase  four  fold  without  a 
corresponding  increase  in  the  pulse  beat.  The  breathing  may 
reach  from  80  to  100  per  minute.  In  character  the  respirations 
are  shallow  on  account  of  the  fixed  condition  of  the  ribs  and 
the  spasms  of  the  muscles  which  compress  the  abdomen. 
There  mav  be  cyanosis  and  catarrh  of  the  nasal  mucosa, 
coughing  and  in  fatal  cases  symptoms  of  hyperaemia  and 
oedema  of  the  lungs  and  often  pneumonia  (usually  aspiration 
in  nature).  There  is  constipation  due  to  lack  of  peristalsis 
and  the  rigid  condition  of  the  muscles  which  compress  the 
abdomen.  Micturition  becomes  less  frequent  and  more  diffi- 
cult. Complete  retention  of  urine  is  said  to  occur  in  some  cases. 
The  urine  has  a  high  specific  gravity  and  in  some  cases  contains 
albumen.  Some  animals  can  eat  readily  while  others  eat,  if  at 
all,  with  great  difficulty.  They  like  to  play  with  drink  set 
before  them  and  often  try  to  satisfy  their  thirst,  which  seems 
to  increase  as  the  disease  advances.  In  fatal  cases  the  animals 
seem  to  be  perfectly  conscious  to  the  last.  They  seem  to  be 
possessed  of  a  feeling  of  terror. 

§147.  Morbid  anatomy.  The  gross  examination  of  the 
tissues  at  post-mortem  of  animals  dead  from  tetanus  is  usuall}' 
negative.  It  has  been  pointed  out  by  Goldscheider  and  Flatau 
that  in  experimental  animals  there  are  certain  characteristic 
changes  in  the  motor  cells  of  the  anterior  horns  ofthe  spinal  cord 
which  in  the  order  of  their  development  depend  upon  the  con- 
centration of  the  toxin  or  virulence  of  the  bacteria  injected 
and  upon  the  duration  of  the  disease.  The  changes  are  pri- 
marily an  enlargement  of  the  nuclei,  which  at  the  same  time 


MORBID    ANATOMY  igi 

become  more  indistinct  ;  then  follows  an  enlargement  and  dis- 
intergration  of  Nissl's  cell-granules  with  an  enlargement  of 
all  of  tlie  nerve  cells.  These  investigators  also  found  that 
where  antitoxin  has  been  used  it  had  a  distinct  retarding  in- 
fluence upon  these  changes.  They  found  like  lesions  in  the 
spinal  cord  of  a  human  subject  dead  of  tetanus.  Very  simi- 
lar results  have  been  obtained  by  Matthes,  Westphal,  Goebel 
and  others.  The  lesions  point  to  the  anterior  horns  of  the 
spinal  cord  as  the  primary  seat  of  origin  of  the  tetanic  contrac- 
tions. The  changes  pointed  out  above  are  said  by  Mo.schowitz 
to  be  characteristic  of  tetanus  and  constantly  found.  The 
motor  ganglia  cells  of  the  anterior  horns  of  the  spinal  cord 
seem  at  present,  therefore,  to  be  the  most  likely  source  of  the 
spasms,  due  apparenth'  to  a  specific  affinity  between  those 
cells  and  the  tetanus  toxin.  It  is  possible  to  explain  also  the 
local  spasms  on  this  hypothesis  as  the  toxin  elaborated  bj'  the 
tetanus  bacilli  is  taken  up  and  carried  to  the  spinal  cord  by  the 
nerves  terminating  in  the  affected  region.  The  experiments 
of  Tizzoni  and  Cattani  suggest  the  possibility  of  such  a  theor}-. 
There  is,  however,  need  for  further  investigation  of  this  subject. 
A  considerable  number  of  lesions  may  be  found  elsewhere 
in  the  body  none  of  which  can  be  considered  as  characteristic  of 
the  disease,  but  which  are  secondary  to  the  tonic  contractions. 
The  blood  owing  to  lack  of  oxidation  may  be  dark  colored, 
tarry,  of  a  greasy  appearance  and  tardy  in  coagulating.  There 
ma3^  be  numerous  ecchymo.ses  and  sanious  exudates  in  the  sub- 
serous and  mucous  membranes.  The  lungs  mav  be  variouslv 
affected  according  to  the  extent  of  the  trouble  with  the  respira- 
tory muscles.  Thus,  congestion,  oedema,  hemorrhages,  pneu- 
monia, emphysema  and  hj-postatic  congestions  have  been  de- 
scribed. In  the  heart  there  are  usually  epi-  and  endocardial 
hemorrhages.  The  muscles  may  contain  hemorrhages.  The 
fibers  of  the  muscles  may  show  cloudy  swelling,  a  loss  of  the 
transverse  striae  and  changes  in  the  nuclei.  The  liver  may 
be  swollen  and  abnormally  yellow  in  color.  The  hepatic  cells 
often  show  fatty  degeneration.  The  spleen  is  often  swollen  ; 
it  may  be  engorged  with  blood  or  soft  and  flabby.  The  kid- 
neys may  or  may  not  show  degenerative  changes.     The  blad- 


192  TETANUS 

der  is  usually  distended  with  urine  and  its  mucous  membrane 
is  often  sprinkled  with  ecchymoses.  The  digestive  tract  may 
show  areas  of  congestion  and  ecchymoses. 

The  course  of  the  disease  varies  in  different  species  and  in 
different  individuals  of  the  same  species.  In  the  horse  it  may 
last  for  two  or  three  days  only  or  it  may  continue  for  several 
weeks.  In  cattle  the  course  is  usually  less  rapid,  but  it  rarely 
runs  longer  than  two  weeks.  In  sheep  it  usually  terminates 
fatally  within  a  week  and  often  in  two  or  three  days. 

§  148.  DifTerential  diagnosis.  Tetanus,  while  possess- 
ing quite  characteristic  symptoms,  may  be  mistaken  for  a 
number  of  other  affections  or  specific  diseases.  Among  those 
which  should  receive  special  attention  are  cerebro- spinal  men- 
ingitis and  rabies  (for  the  symptoms  and  lesions  see  those  dis- 
eases). Rheumatism,  eclampsia,  catalepsy,  convulsions  in  the 
newly  born  and  pyaemic  polyarthritis  in  lambs  and  foals. 

The  symptoms  of  tetanus  which  are  perhaps  the  most 
diagnostic  are  (i)  the  continuous  tonic  spasms  of  different 
groups  of  muscles,  (2)  the  apparent  clearness  of  mind,  (if  we 
may  attribute  such  a  quality  to  animals)  and  (3)  the  absence 
of  fever  in  the  beginning  of  the  S5miptoms.  The  general  atti- 
tude of  the  animal  is  also  of  much  value.  If  the  infected 
wound  can  be  found  it  is  often  possible  to  obtain  coverglass 
preparations  in  which  the  tetanus  bacilli  can  be  found.  Nega- 
tive results  are  in  this  case  not  to  be  considered  as  final  for  it 
is  practically  impossible  to  make  these  examinations  suiSci- 
ently  thorough  to  be  sure  of  the  absence  of  these  bacilli,  if 
they  are  not  found.  If  they  are  found  the  diagnosis  ma}-  be 
considered  as  positive. 

In  poisoning  with  strychnine,  there  are  symptoms  which 
at  first  may  be  more  confusing.  This  form  of  poisoning 
usually  occurs  in  dogs  where  tetanus  is  rare  and  again  in 
strychnine  poisoning  the  suddenness  of  the  attack,  the  rapidity 
of  the  cour.se  and  the  increased  reflex  irritability  are  valuable 
diagnostic  features.  In  differentiating  tetanus  from  other 
affections  as  those  in  the  newly  born,  the  bacteriological  exam- 
ination of  preparations  made  from  the  end  of  the  umbilicus  may 
be  of  much  assistance. 


PREVENTION  I93 

§  149.  Prevention.  Owing  to  the  wide  distribution  of 
tetanus  bacilli,  precautions  can  consist  only  of  the  careful  and 
thorough  disinfection  of  all  wounds.  With  animals  at  pas- 
ture, it  is  impossible  often  to  know  of  the  wounds  until  it  is 
too  late  to  apply  this  measure.  In  stables  where  the  disease 
becomes  prevalent,  the  floors  and  siding  should  be  thoroughly 
disinfected  and  special  watchfulness  exercised  to  find  at  the 
earliest  moment  any  injury  by  which  infection  could  occur. 
The  practitioner  should  learn  as  soon  as  possible  the  tetanus 
infected  lands  and  stables  in  his  commnity  and,  knowing 
these,  give  wise  instruction  to  his  clients  to  take  such  precau- 
tions as  are  possible.  If  the  present  knowledge  of  this  disease 
is  properly  availed  of,  there  should  be  only  occasional  cases 
which  as  yet  there  seems  to  be  no  way  to  avoid. 

§  150,  Tetanus  antitoxin.  It  was  first  pointed  out  by 
Behring  and  Kitasato  that  animals  could  be  made  immune  to 
tetanus  by  using  cultivations  of  the  tetanus  bacilli  which  had 
been  attenuated  with  iodine  trichloride.  The  blood  serum  of 
such  immunized  animals  has  the  power  to  immunize  healthy 
animals  against  the  disease  and  to  render  the  toxin  in  animals 
affected  with  tetanus  inert.  The  antitoxin  is  prepared  now, 
however,  by  injecting  horses  with  the  filtrate  of  bouillon 
cultures,  either  alone  or  with  a  quantity  of  antitoxin.  After 
the  first  dose  the  animal  becomes  tolerant  to  a  certain  degree 
so  that  by  repeated  and  constantly  increasing  doses  complete 
resistance  to  the  toxin  is  acquired.  When  this  point  is  reached 
the  serum  usually  possesses  a  strong  antitoxin  power.  As  a 
practical  remedy  for  the  disease  in  animals  the  recorded  results 
from  the  use  of  this  antitoxin  are  somewhat  contradictory.  In 
human  practice  the  results  are  similar.  Moschcowitz  has  col- 
lected 290  cases  in  man,  where  it  has  been  used  subcutaneously 
with  173  recoveries  and  117  deaths  or  amortality  of  40.33  per 
cent.  In  a  total  of  48  cases  where  the  antitoxin  has  been  injected 
intracerebrally  23  recovered  and  25  died,  a  mortality  of  52.08 
percent. 

Some  interesting  experiments  suggested  by  Krokiewitz 
directed  toward  the  finding  of  a  specific  treatment  consist  in 
the  injection   of  an   emulsion   of  brain   substance.      Primarily 


I 94  TETANUS 

this  method  of  treatment  is  based  upon  the  hypothesis,  set  up 
by  Goldscheider  and  Flatau,  who,  as  a  result  of  their  research 
came  to  the  conclusion  that  "The  morphological  changes  in 
the  nerve  cells  are  the  expression  of  a  chemical  process,  i.  e., 
of  the  chemical  combination  of  the  toxins  with  the  nerve 
cells.  Every  nerve  cell  possesses  atom  groups  which  have  a 
certain  affinity  for  the  atom  groups  of  the  tetanus  toxin  and 
are  able  to  combine  with  them."  Wassermann  and  Takaki 
substantiated  this  hypothesis  experimentally  ;  these  observers 
injected  into  experimentally  tetanized  animals  an  emulsion  of 
spinal  cord,  obtained  from  a  freshly  killed  animal,  to  test,  if 
possible,  whether  the  nerve  cells  of  the  dead  animal  also  have 
this  affinity  for  the  tetanus  toxin,  like  the  nerve  cells  of  the 
living  animal.  By  this  experiment,  they  have  come  to  the 
conclusion  that  every  part  of  the  nervous  system,  particularly 
the  brain  of  the  examined  animals  including  man,  has  a 
definite  and  positive  tetanus  antitoxic  power  ;  and  that  the 
injection  of  normal  brain  substance  into  experimentally 
tetanized  animals  has  the  power  to  save  life.  Further  work  in 
this  direction  is  necessary  to  fully  demonstrate  the  efficiency 
of  this  procedure. 

REFERENCES. 

.  I.  Behring  and  KiTASATo.  Ueber  das  Zustandekoninien  der 
Diphtheric — Immunitat  und  der  Tetanus — Immunilat  bei  Thieren. 
Deutsche  Med.   Wochenschrift.     Bd.  XVI.   (1890)  S.  113. 

2.  KiTASATo.  Ueber  den  Tetanusbacillus.  Zeit.f.  Hygiene.  Bd. 
VII.  (1889)  S.  225. 

3.  KiTASATO.  Experimentelle  Untersuchungen  iiber  das  Tetanus- 
gift.     Zeit.f.  Hygiene.     Bd.  X.  (1891 )  S.  267. 

4.  MosCHCOWiTZ.  Tetanus,  a  study  of  the  nature,  excitant,  lesions, 
symptomatology,  and  treatment  of  the  disease,  with  a  critical  summary 
of  the  results  of  serum  therapy.  Studies  from  the  Department  of  Path- 
ology of  the  College  of  Physicians  and  Surgeons,  Columbia  University. 
Vol.  VII.  (1899-1900).  (M.  gives  pathology  and  antitoxin  treatment, 
summary  of  cases  and  full  bibliography. ) 

5.  iviCFARLAND.  Tetanus  and  vaccination.  The  Journal  of  Medi- 
cal Research.     Vol.  VII.   (1902)  p.  474. 


HISTORY  195 

SYMPTOMATIC  ANTHRAX. 

Synonyms.  Black  quarter  ;  black  leg  ;  quarter  ill  ;  quar- 
ter evil  ;     Charbon  sympiomatiqiie  ;  Rauschbrand. 

§151.  Characterization.  Black  quarter  is  an  acute  in- 
fectious disease  of  cattle  characterized  by  the  development  of 
an  emphysematous  .swelling  of  the  subcutaneous  tissues  and 
muscles.  The  lesions  are  usually  located  upon  and  ordinarily 
•extend  over  the  greater  part  of  a  hind  quarter  or  a  shoulder. 
The  disease  does  not  spread  from  animal  to  animal  by  simple 
contact  but  the  infection  takes  place  apparently  from  a  com- 
mon source,  the  soil.  The  virus  seems  to  exist  in  the  soil  in 
•certain  localities  only.  "  Like  tetanus,  it  is  a  disease  following  a 
wound  infection. 

Symptomatic  anthrax  is  a  disease  of  cattle,  sheep  and  goats 
although  the  two  latter  species  are  rarely  attacked.  Guinea 
pigs  are  very  susceptible  to  inoculation.  It  is  reported  that 
horses,  asses  and  white  rats  develop  local  lesions  when  inocu- 
lated subcutaneou.sly  with  the  virus.  Other  animals  seem  to 
be  immune.  In  cattle,  it  rarely  occurs  in  the  very  young, 
under  six  months,  and  in  adults  after  the  fourth  year. 

§  152.  History.  It  is  supposed  that  black  quarter  has 
•existed  for  hundreds  of  years  although  it  was  not  until  late  in 
the  last  century  that  it  was  positively  differentiated  and  recog- 
nized as  a  distinct  and  specific  disease.  The  descriptions  given 
in  many  of  the  earlier  epizootics  designated  as  anthrax  corre- 
spond more  exactly  with  the  present  knowledge  of  black  quarter 
than  they  do  of  anthrax. 

In  1782,  Chabert  classified  the  various  anthracoid  diseases 
recognized  at  that  time,  into  three  groups,  viz.:  (i)  anthrax 
fever  or  where  the  disease  manifested  itself  without  external 
swelling  ;  (2)  true  anthrax,  or  where  the  lesions  consisted  at 
first  of  small,  hard  and  very  painful  swellings  followed  or 
accompanied  by  fever  and  other  general  symptoms  and  (3) 
symptomatic  anthrax  or  where  the  swelling  was  preceded  by 
a  rise  of  temperature,  loss  of  appetite  and  .symptoms  of  general 
•depression.  This  classification  obtained  for  nearly  a  century. 
Eoutrolle,  in  1797,  refers  to   a  disease  which  he  called  vial  de 


196  SYMPTOMATIC    ANTHRAX 

cuisse  (quarter  evil)  because  it  affected  the  animal  in  the  thigh. 
Viborg  described  the  disease  in  Denmark  where  it  has  long 
been  known  to  the  laymen  and  designated  by  them  as  raslesyge 
("rattle  disease").  Its  clinical  features  were  very  accurately 
described  b}-  Walrafifin  1856.  In  1879,  Arloing,  Cornevin  and 
Thomas  proved  the  causal  relations  of  a  certain  microorganism 
to  this  disease  and  thus  established  its  specific  nature.  A 
year  later,  1880,  they  described  the  specific  microorganism  and 
demonstrated  that  the  disease  could  be  produced  by  inoculat- 
ing susceptible  animals  with  it.  Since  that  time  both  the 
organism  and  the  disease  itself  have  been  studied  by  many 
investigators.  In  this  country,  the  disease  has  been  under 
investigation  during  the  last  few  years  by  investigators  in  the 
Bureau  of  Animal  Industry. 

§  153.  Geographical  distribution.  Black  quarter  ex- 
ists to  some  extent  in  nearly  every  country  in  the  world.  It 
is  reported  as  occurring  in  the  most  northern  latitudes  in  which 
cattle  are  kept,  as  well  as  in  the  tropical  and  temperate  zones. 

In  Europe,  it  occurs  on  the  pastures  on  the  Alps,  where 
for  five  months  in  the  year  the  ground  is  covered  with  snow 
and  ice  and  in  America  it  is  quite  common  in  certain  northern 
districts.  It  has  been  reported  from  Asia  and  from  Northern 
and  Southern  Africa. 

In  the  United  States,  it  prevails  to  a  greater  extent  than 
is  generally  supposed.  The  states  and  territories  which, 
according  to  the  reports  of  the  Bureau  of  Animal  Industry, 
suffer  most  from  it  are  Texas,  Oklahoma,  Kansas,  Nebraska, 
Colorado,  North  and  South  Dakota  and  Indian  Territory  bui 
a  number  of  the  other  Western  States  are  badly  affected. 
Many  of  the  states  east  of  the  Mississippi  river  have  infected 
localities,  but  in  a  few  of  the  eastern  and  southern  states  it 
seems  not  to  exist.  During  the  last  tew  years  infected  locali- 
ties have  been  found  in  New  York  where  there  has  been 
an  annual  loss  from  this  disease,  but  where  prior  to  recent  in- 
vestigations the  cause  of  death  had  been  attributed  to  poisoning. 

>^  154.  Etiology.  Black  quarter  is  caused  by  a  motile, 
rod-shaped  microorganism  varying  from  3  to  5//  in  length  and 
from  0.5  to  i.o/<    in  width.     The    ends   are    rounded  and  it 


SYMPTOMS  197 

produces  spores.     In  cultures  long  involution  fornis^are  often 

observed.       It  is  anaerobic  and  consequently  will^not  develop 

in  the  presence  of  air.    In  suitable  culture  media  under  anaerobic 

conditions  or  in  animal  tissues  (other  than  blood)  itnuultiplies 

rapidly  with    the    evolution    of    gas.     The 

presence  of  spores  renders  it  very  resistant        ^      ^ 

to  natural  destructive  agencies  and  to  the         ©  ^    if 

common  disinfectants.    The  bacillus  of  black       j  a  /^      ® 


quarter  or  its   spores  are  supposed  to  gain      -  ^  ^        f    ssza 
entrance  to  the  tissues  of  animals  through 
abrasions  of  the  skin  or,  possibly,  the  mucous 
membranes  of  the  mouth  or  intestine.  Fig.    43.     Ba- 

§155.  Symptoms.  Black  quarter  runs  cillus  of  symptoma. 
a  rapid  course  and  usually  ends  fatally  in  • 
from  one  to  three  days.  The  first  symptoms  may  be  either 
general  or  local  in  character.  Arloing,  Cornevin  and  Thomas 
believe  that  general  symptoms  always  precede  the  local  mani- 
festations. Norgaard  reports  finding  cattle  with  marked  local 
lesions  but  few  animals  suffering  from  general  symptoms  al- 
though the  latter  may  have  preceded  the  former  and  have 
subsided. 

The  general  symptoms  are  elevation  of  temperature, 
which  usually  falls  to  the  normal  or  even  subnormal  before 
death,  loss  of  appetite,  loss  of  rumination  and  pronounced 
depression.  Respiration  becomes  accelerated,  the  animal 
moves  with  difficulty  and  lies  down  frequently.  At  first  the 
visible  mucous  membranes  are  congested  and  within  twelve  to 
fifteen  hours  they  have  a  dirty  leaden  or  purplish  color. 

The  local  symptoms  may  appear  on  different  parts  of  the 
body  except  below  the  knee  or  hock  joints  and  on  the  tail. 
They  are  less  frequently  found  about  the  head.  They  usually 
appear  on  the  thighs,  neck,  shoulders  and  lower  region  of  the 
chest.  The  swelling  is  at  first  small  and  painful.  It  spreads 
rapidh'  and  may  in  a  few  hours  attain  to  a  large  size  when  it 
becomes  characterized  by  a  crackling  and  gurgling  sound 
when  the  hand  is  passed  over  it.  On  percus.sion  it  gives  a 
clear,  tympanic  sound  due  to  the  collection  of  gas  in  the 
affected  tissues.      At   the  center  of    the   larger  swellings  the 


igS  SYMPTOMATIC    ANTHRAX 

skin  becomes  dry  and  parchment  like,  cool  to  the  touch  and 
painless  upon  pressure.  If  lanced,  a  dark  reddish,  frothy 
fluid  flows  from  the  wound.  It  emits  a  disagreeable  odor. 
In  some  cases  there  is  but  one  swelling  but  usually  there  are 
two  or  more  which  may  become  confluent.  The  lymph  glands 
adjacent  to  the  swellings  are  much  enlarged. 

Hun  has  pointed  out  the  interesting  fact  that  in  a  very 
large  percentage  of  cases  the  swellings  appear  on  the  right 
side.  There  seems  to  be  no  explanation  given  for  this  localiza- 
tion. In  this  country,  records  are  wanting  of  observations  on 
this  point. 

Arloing  has  called  attention  to  a  mild  form  of  this  disea.se 
in  which  the  symptoms  are  slight  debility,  loss  of  appetite  and 
slight  local  swelling. 

§  156.  Morbid  anatomy.  After  death  the  carcasses  of 
animals  which  have  died  of  this  disease  soon  become  distended 
with  gas.  This  is  due  in  part  to  the  fermentation  in  the 
digestive  tract  and  in  part  to  the  formation  of  gas  in  the  sub- 
cutaneous tissues  due  to  the  presence  of  the  specific  bacillus. 
The  subcutaneous  distension  is  especially  marked  in  the  region 
of  the  swellings  but  it  extends  for  a  considerable  distance  from 
these  foci  in  the  direction  of  least  resistance.  The  tympanitic 
condition  often  causes  the  two  legs  on  the  upper  side  of  the 
carcass  to  extend  out  straight  without  touching  the  ground. 
A  dark,  blood-colored,  frothy  discharge  flows  from  the  nostrils 
and  anus.  Decomposition  takes  place  very  rapidl}'  except  in 
the  affected  muscles  which  retain  a  sweetish-sour  odor  for  a 
considerable  time  after  other  parts  of  the  carcass  have  become 
putrid. 

The  skin  covering  the  swellings  is  often  affected  with  dry 
gangrene.  The  subcutaneous  connective  tissue  is  yellow,  gelat- 
inous, infiltrated  with  blood  and  bubbles  of  gas  which  escape  if 
the  tumor  is  incised.  The  muscles  underneath  the  tumors  are  of 
a  dirty  brown  or  of  a  blackish  color.  At  other  places  they 
are  dark  red  or  dark  yellow  and,  when  exposed  for  some  time 
to  the  air,  they  may  have  a  golden  lustre.  The}'  are  brittle, 
putrid  and  very  rich  in  fluids.  They  crackle  on  palpation. 
When    incisions    are    made    into    them,   blood    of    a    frothy, 


MORBID    ANATOMY  199 


greasy,  tarry  appearance  and  of  a  sickish,  foetid  odor  issues 
from  them  when  they  are  squeezed.  The  fibres  of  the  muscles 
show  extremely  varied  degenerative  changes.  The  gases  that 
are  present  in  the  muscles  are  inflammable  and  burn  with  a 
bluish  flame  on  being  ignited.  They  are  stated  to  have  but 
little  odor,  on  which  account  it  is  assumed  that  they  consist  of 
carburetted  hydrogen.  They  are  also  said  to  contain  carbonic 
acid  but  no  oxygen.  An  exact  chemical  analysis  of  these 
gases  seems  not  to  have  been  made.  The  lymph  glands  near 
the  tumors  are  enlarged  and  full  of  blood.  They  contain 
hemorrhages  and  are  infiltrated  with  a  serous  fluid.  The 
afferent  lymph  vessels  are  sometimes  distended  with  gases, 
giving  them  the  appearance  of  strings  of  beads.  Changes 
similar  to  those  of  the  external  muscles  appear  in  the  muscles 
of  the  tongue  and  pharynx  when  the  disease,  as  may  happen 
in  rare  cases,  is  localized  in  the  oral  and  pharyngeal  mucous 
membranes. 

A  large  amount  of  blood-red  exudate  is  frequently 
found  in  the  abdominal  cavity.  In  other  cases  only  small 
quantities  of  a  serous  fluid  is  present.  In  still  others  no 
changes  at  all  appear.  The  abdominal  changes  seem  to  be 
determined  by  the  swelling  of  the  muscles,  /.  e.,  whether  it  has 
or  has  not  spread  to  the  peritoneum.  Yellow  gelatinous  and 
hemorrhagic  infiltrations  are  often  met  with  on  the  omentum, 
mesentery  and  in  the  neighborhood  of  the  kidneys.  The 
mucous  membrane  of  the  stomach  and  small  intestine  is  fre- 
quently swollen,  congested  and  infiltrated  with  hemorrhages, 
in  which  case  the  contents  of  the  intestine  are  bloody.  The 
liver  is  hyperemic,  but  the  spleen  is  usually  normal. 

In  the  thoracic  cavity,  the  pleurae  in  the  neighborhood  of 
the  swollen  parts  of  the  skin  and  mediastinum  are  sometimes 
hemorrhagic.  The  pleurae  may  also  show  large  ecchymoses, 
in  which  case  the  thoracic  cavity  contains  a  sero-sanious  exu- 
date. Hemorrhages  are  sometimes  present  in  the  lungs,  peri- 
cardium, myocardium  and  under  the  endocardium.  The 
muscular  tissue  of  the  heart  is  very  soft,  but  the  other  muscles 
show  only  slight  changes.      The    mucous   membrane    of  the 


200  SYMPTOMATIC    ANTHRAX 

bronchi  are  sometimes  hyperemic  and  sprinkled  with  hemor- 
rhages. 

The  blood  is  of  a  normal  color  and  coagulates  readily. 
The  fluids  of  the  muscles  have,  according  to  Feser,  an  acid 
reaction,  and  the  flesh  becomes  rapidly  putrid.  The  bacilli  of 
quarter-ill  are  found  only  in  small  numbers  if  at  all  in  the 
blood  during  life,  but  abundantly  a  few  hours  after  death. 
They  are  numerous  in  the  local  lesions. 

§  157.  Differential  diagnosis.  Black  quarter  is  to  be 
differentiated  from  anthrax,  the  "corn-stalk"  disease,  septi- 
caemia hemorrhagica  and  various  forms  of  poisoning.  Usually 
the  localized  subcutaneous  lesions  are  sufficient  to  differentiate 
black  quarter  from  these  other  affections.  It  often  happens, 
however,  that  post-mortem  changes  have  so  modified  the  car- 
cass before  it  can  be  examined  that  the  diagnosis  is  question- 
able. In  this  and  all  doubtful  cases  or  where  only  small 
portions  of  tissue  are  sent  for  examination,  it  is  necessary  to 
resort  to  a  more  definite  method  or  methods,  viz. :  microscopic 
examination,  cultures  and  animal  inoculation. 

(i)  Microscopic  examinatioji.  Cover-glass  preparations 
made  from  the  fresh  tissues  will  ordinarily  exhibit  the  specific 
bacteria.  They  are  easily  distinguished  m  case  of  anthrax  and 
black  quarter  and  often  with  septicaemia  hemorrhagica  while 
in  the  "corn-stalk"  disease  and  cases  of  poisoning  charac- 
teristic bacteria  are  not  found.  It  is  important  to  eliminate 
putrifactive  bacteria,  when  the  animals  have  been  dead  for 
some  hours. 

(2)  CulUires.  Ordinary  culture  media  inoculated  with 
the  tissues  from  a  case  of  anthrax  will  give  growths  of  the 
anthrax  bacterium,  and  from  cases  of  septicaemia  hemorrha- 
gica that  of  B.  bovisepticus,  but  with  the  other  two  diseases 
they  will  remain  clear  if  uncontaminated.  The  black  quarter 
bacillus  will  grow  on  these  media  only  when  placed  in  anaero- 
bic conditions.  In  case  of  the  "corn  stalk"  disease  the  media 
will  continue  to  be  clear. 

(3;  Animal  i^ioculation.  In  guinea-pigs  inoculated  in  the 
deeper  subcutaneous  tissues  wnth  pure  cultures  of  sympto- 
matic anthrax  bacteria  or  with  bits  of  tissue  from  the  affected 


PREVENTION  20I 

area  of  another  animal  dead  from  the  disease,  death  ensues 
in  from  one  to  two  days.  It  is  preceded  by  rise  of  tempera- 
ture, loss  of  appetite  and  general  indisposition.  The  site  of 
inoculation  is  swollen  and  painful  and  drops  of  bloody  serum 
may  sometimes  be  seen  exuding  from  it.  At  autopsy  the  sub- 
cutaneous cellular  tissues  and  underlying  muscles  present  a 
condition  of  emphysema  and  extreme  oedema.  The  oedema- 
tous  fluid  is  often  blood  stained  and  the  muscles  are  of  a  blackish 
or  blackish  brown  color.  The  lymphatic  glands  are  markedly 
hyperaemic.  The  internal  viscera  present  but  little  alteration 
visible  to  the  naked  eye.  In  the  blood  stained  serous  fluid  about 
the  point  of  inoculation  short  bacilli  are  present  in  large 
numbers.  These  often  present  slight  swellings  at  the  middle 
or  near  the  end.  They  are  not  seen  as  threads  but  lie  singly 
in  the  tissues.  If  the  autopsy  is  made  immediately  after 
death,  these  organisms  may  not  be  detected  in  the  internal 
organs,  but  if  not  made  until  after  a  few  hours,  they  will  be 
found  there  also.  In  recent  autopsies  only  the  vegetative 
forms  of  the  organism  may  be  found,  but  later  (in  from 
twenty  to  twenty- four  hours)  spore-bearing  rods  may  be 
detected.  With  the  "corn-stalk"  disease  the  inoculated 
animals  will  remain  well. 

§  158.  Prevention.  In  checking  the  spread  of  the 
disease  it  is  very  important  wherever  it  is  possible  to  remove 
the  well  animals  from  the  infected  field  and  to  restrict  the  sick 
ones  to  a  small  one.  The  swellings  should  not  be  opened  and 
the  discharge  scattered  over  the  field.  The  dead  animals 
should  be  burned  if  possible,  otherwise  buried  deeply  and 
covered  well  with  lime  as  soon  as  possible  after  death.  Birds 
and  other  animals  should  not  be  allowed  to  feed  upon  the  car- 
casses and  the  skin  should  not  be  removed.  Every  precaution 
to  restrict  the  spread  of  the  bacteria  of  this  disease  should  be 
taken.  It  is  very  desirable  to  thoroughly  disinfect  the  ground 
where  the  animal  lay  at  the  time  of  death.  The  spores  are 
very  resistant  both  to  disinfectants  and  the  natural  destructive 
agencies  such  as  sunlight  and  drying.  It  is  not  wise  to  use 
land  for  grazing  purposes  for  susceptible  species  upon  which 
animals  have  contracted  the  disease. 


202  SYMPTOMATIC    ANTHRAX 

§  159.  Preventive  inoculation.  Several  methods  of 
fortifying  exposed  animals  against  the  infection  of  sympto- 
matic anthrax  virus  have  been  proposed.  In  1880,  Arloing, 
Cornevin  and  Thomas  demonstrated  at  Chaumont  that  animals 
injected  with  the  filtrate  of  cultures  of  this  virus  into  the  jugu- 
lar vein  were  protected  against  inoculation  with  the  strong 
virus.  It  was  found,  however,  that  this  method  was  difficult 
as  the  vein  had  to  be  exposed  and  the  greatest  care  was  neces- 
sary to  prevent  infection  of  extra  vascular  tissue  in  introduc- 
ing and  withdrawing  the  syringe.  Later  these  investigators 
attenuated  the  virus  b}-  heating  it  to  a  temperature  of  100  to 
104°  C.  and  injecting  it  into  the  subcutisof  the  shoulder.  This 
gave  a  partial  immunity  which  was  reinforced  after  eight  or 
ten  days  by  a  second  inoculation  of  a  virus  that  had  been 
heated  from  90  to  94°  C.  for  six  hours.  They  injected  the 
virus  where  the  subcutis  is  quite  dense,  such  as  at  the  end  of 
the  tail  where  only  local  swellings  would  occur.  This  process 
is  known  as  "the  French  method  "  Arloing's  method  or  the 
"  Lyons  method." 

In  1S88,  Kitt,  of  the  Veterinary  College  in  Munich,  after 
a  careful  investigation  of  the  subject  proposed  a  single  injec- 
tion method  using  a  virus  attenuated  bj-  heating  at  a 
temperature  of  from  85  to  90°  C.  for  six  hours.  A  single  in- 
jection of  this  vaccine  would  usually  confer  immunit}'.  He 
further  modified  Arloiug's  method  by  making  the  injections  in 
the  shoulder  region  where  the  skin  is  looser  and  the  operation 
easier.  Later,  Kitt  made  further  important  investigations 
concerning  preventive  vaccines  for  this  disease. 

In  the  fall  of  1896,  investigations  preparatory  to  the  prepa- 
ration of  a  black  quarter  vaccine  were  begun  in  the  Bureau  of 
Animal  Industry  at  Washington  b}-  Dr.  Norgaard  under  the 
direction  of  Dr.  D.  E.  Salmon.  The  various  European 
methods  were  tried.  The  one  finalh'  adopted  consists  of  a 
single  vaccine,  the  Arloing  principle,  with  Kitt's  modification. 

The  material  used  for  the  vaccine  is  obtained  from  a  fresh, 
blackleg  tumor,  b}'  pounding  the  muscle  tissue  in  a  mortar 
with  the  addition  of  a  little  water  and  .squeezing  the  pulp 
through  a  piece  of  linen  cloth.      The  juice  is  spread  in  layers 


PREVENTIVE    INOCULATION  2.03 

on  plates  and  dried  quickly  at  a  temperature  of  about  35°  C. 
This  temperature  does  not  in  the  least  affect  the  bacteria,  and 
the  dry  virus  obtained  in  this  way  retains  a  high  degree  of 
virulence  for  two  years  or  longer. 

When  vaccine  is  to  be  prepared,  the  dried  material  is  pul- 
verized and  mixed  in  a  mortar  with  two  parts  water  until  it 
forms  a  semifluid  homogeneous  mass.  This  is  spread  in  a  thin 
layer  on  a  suitable  glass  dish,  and  placed  in  an  oven,  the 
temperature  of  which  may  be  regulated  with  exactness.  The 
reason  for  mixing  the  dried  muscle  with  water  is  to  insure  a 
quicker  and  more  uniform  attentiation.  The  temperature  of 
the  oven  is  previously  brought  up  to  95°  to  99°  C,  and  the 
virus  is  allowed  to  remain  in  it  for  six  hours.  When  removed 
it  appears  as  a  brownish  scale,  which  is  easily  detached  from 
the  dish.  This  scale  is  pulverized  and  put  up  in  packets  con- 
taining 10  doses  each.  Before  it  is  used,  it  is  mixed  with 
10  c.c.  of  water  filtered  and  the  filtrate  injected  in  doses  of 
one  cubic  centimeter. 

REFERENCES. 

1.  Fisher.  Blackleg  in  Kansas,  and  protective  inoculation. 
Kan.  State  Agric.  Exper.  Station.     1901. 

2.  Lewis  Symptomatic  anthrax.  Bulletin  No.  2j.  Oklahoma 
State  Agric.  Expe7\  Station.     1897. 

3.  Mayo.  Blackleg.  Bulletin  No.  6g.  Kan.  State  Agric.  Expt. 
Station.      1897,  p.  108. 

4.  NoRGAARD.  Blackleg  in  the  United  States  and  the  distribution 
of  vaccine  by  the  Bureau  of  Animal  Industry.  Annual  Report  of  the 
Bureau  of  Annual  Industry,  U.  S.  Dept.  Agric.     1898. 

5.  NoRGAARD.  Blackleg.  Its  nature,  cause,  and  prevention. 
Ibid.     Circular  No.  23.     U.  S.  Bureau  of  Animal  Industry.     1S98. 

6.  Peters  Blackleg.  Its  nature,  cause,  and  prevention.  Bulle- 
tin No.  65.     Neb.  State  Agric.  Exper.  Station.     1900. 

7.  Salmon.  Black  quarter.  Annual  Report  Bureau  of  Animal 
Industry.      U.  S.  Dept.  of  Agriculture.     1893-4. 


CHAPTER  V 


DISEASES   CAUSED  BY  FUNGI. 

ACTINOMYCOSIS. 

Synomyms,     Lumpy  jaw  ;    Wooden  tongue  ;    Big  head. 

§  i6o.  Characterization.  Actinomycosis  belongs  to  the 
•class  of  affections  known  as  the  infectious  granulomata.  It  is 
a  chronic  disease  determined  by  the  presence  of  a  specific 
cause— the  ray  fungus— which  by  irritation  stimulates  the  for- 
mation of  new  growths  consisting  of  round  cells,  epithelioid 
cells,  giant  cells  and  fibrous  tissue.  The  neoplasms  appear  as 
tumors  having  either  a  tendency  to  develop  into  large  and 
hard  masses  or  to  suppurate.  It  has  been  suggested  that  the 
suppuration  was  due  to  a  secondary  infection  by  p30genic 
bacteria. 

Cattle  (genus  Bos)  are  most  often  attacked.  Men  are 
susceptible  but  the  disease  is  rarely  found  in  the  human  sub- 
ject. Horses,  dogs,  pigs,  sheep  and  elephants  are  slightly 
susceptible  and  a  few  cases  have  been  reported  in  each.  Other 
species  seem  to  be  immune. 

§  i6i.  History,  The  early  history  of  this  disease  is  quite 
obscure.  Prior  to  the  discovery  of  its  specific  cause  it  was 
much  confused  with  other  diseases  resembling  it  more  or  less 
closely  in  certain  gross  appearance.  It  was  designated  by  a 
variety  of  names,  the  more  common  of  which  are  swelled  head, 
lumpy  jaw,  big  head,  fibroma,  sarcoma  and  osteosarcoma.  It 
is  popularly  known  in  the  United  vStates  as  "lumpy  jaw"  and 
in  Europe  as  "wooden  tongue."  The  popular  names  were 
probably  suggested  by  the  character  of  the  lesions  which  differ 
to  a  marked  degree.  It  was  recognized  as  a  specific  disease  by 
Rivolta  in  iS68,  by  Perroncito  in  1S75  and  by  Bollinger  in 
1877.     The  ray  fungus  was  undoubtedly  observed  prior  to  this 


GEOGRAPHICAL    DISTRIBUTION  205 

by  Lebert  and  Robin  both  of  whom  failed   to   recognize  it  as  a 
vegetable  parasite. 

The  fungus  was  carefully  described  by  Dr.  Harz,  a  botan- 
ist, who  gave  it  the  name  actinomyces  or  ray  fungus.  Bol- 
linger was  the  first  to  carefully  study  the  disease  in  cattle  and 
to  demonstrate  the  power  of  the  ray  fungus  to  produce  di.s- 
ea.se.  With  this  discovery  of  Bollinger  in  1877,  actinomycosis 
became  recognized  as  a  definite,  specific  disease  which  could 
in  most  cases  at  least  be  differentiated  from  the  other  affec- 
tions with  which  it  had  hitherto  been  confused.  In  1845,  von 
Langenbeck  of  Kiel  observed  and  made  drawings  of  peculiar 
bodies  in  a  case  of  vertebral  caries  in  man  which  it  is  now  be- 
lieved were  ro-settes  of  the  ray  fungus.  In  1878  Israel  demon- 
strated the  disease  in  man.  Since  that  time  it  has  been  care- 
fully studied  and  described  by  a  number  of  investigators. 

g  162.  Geographical  distribution.  Actinomycosis  is 
quite  widely  distributed  throughout  North  and  South  iVmerica 
and  Europe.  It  is  much  more  prevalent  in  certain  countries 
and  districts  than  in  others.  The  observation  has  been  made 
that  animals  pastured  upon  low  lands  and  in  river  valleys  are 
more  liable  to  contract  it  than  those  feeding  upon  high  and 
dry  ground.  It  has  also  been  noted  that  cattle  fed  upon 
rough  or  coarse  forage  are  more  prone  to  the  disease  on 
account  of  abrasions  of  the  buccal  mucosa  than  those  kept 
upon  less  harsh  food. 

It  is  very  difficult  to  procure  reliable  statistics  concerning 
the  extent  to  which  it  occurs.  The  observations,  which  have 
been  made  at  the  union  stock  yards,  Chicago,  show  one  case 
of  actinomycosis  in  from  1600  to  1700  cattle.  The  statistics 
from  the  abattoirs  in  Berlin  show  one  case  to  4250  cattle  and 
one  in  Sooo  pigs.  These  figures  do  not,  however,  indicate  the 
extent  of  the  disease  among  the  farm  animals  as  they  are  col- 
lected from  those  animals  presented  for  slaughter  only.  At 
the  clinic  of  the  New  York  State  Veterinary  College  there  is 
presented  for  treatment  a  very  few  cases  each  year.  In  the 
Mississippi  valley  and  in  the  south-w^est  it  seems  to  be  more 
prevalent  than  it  is  east  of  the  Alleghany  Mountains. 


2o6 


ACTINOMYCOSIS 


Fig.  44.    77?^'  ray  fungus. 


§  163.  Etiology.  Actinomyco- 
sis is  produced  by  a  fungus — Clado- 
thrix  adviomyces  commonly  known 
as  the  "  ray  fungus."  The  disease  is 
the  result  of  its  multiplying  in  the  tis- 
sues and  not  from  the  elaboration  of  a 
toxin.  The  fungus  appears  in  minute, 
yellowish  granules  in  the  lesions. 
When  examined  microscopically,  these 
granules  are  found  to  be  made  up  of 
rosettes  varjnng  in  size  from  10  to 
200//  in  diameter.  The  average  size 
ranging  from  30  to  40/<.  This  fungus  can  be  cultivated  on 
artificial  media.  It  stains  somewhat  feebly  with  the  aniline 
dyes. 

The  rosettes  are  composed  of  a  number  of  club-shaped  struct- 
ures (rays),  radiating  from  the  central  mass  which  is  composed 
of  the  mycelial  part  of  the  fungus.  The  club-shaped  bodies 
vary  in  size  but  usually  they  are  from  i  to  lOyu  long.  The 
rays  are  connected  with  the  central  portion  by  fine  thread-like 
structures  which  are  not  readily  demonstrated.  In  tearing  or 
crushing  the  rosette,  tlie  clubs  break  off  at  or  near  their  junc- 
tion with  the  mycelial  threads.  Some  investigators  have  men- 
tioned a  polymorphous  form  of  actinomyces  in  which  coccoid 
and  rod-shaped  structures  are  found.  These  are  doubtless  the 
ends  of  the  clubs  which  first  appear  in  focusing  on  a  rosette. 

The  mycelial  threads  are  wider  in  some  portions  than  in 
others.  In  the  narrowest  places  the  walls  seem  to  touch  each 
other.  Whether  this  irregularity  is  natural  or  the  result  of 
twisting  the  mycelial  thread  is  not  determined.  The  my- 
celium is  much  more  difficult  to  stain  than  the  clubs.  In  some 
cases  it  seems  to  branch.  The  filaments  can  rarely  be  seen  in 
the  rosettes  as  they  occur  in  the  suppurating  lesions. 

The  natural  habitat  of  this  fungus  is  said  to  be  on  certain 
plants.  According  to  Brazzola,  they  vegetate  on  the  grasses 
chiefly  on  Hordeum  imirimirn.  He  di.scovered  quantities  of 
the  fungi  between  the  vegetable  fibres  of  barley  which  were 
imbedded  in  the  gums  of  animals.     Johne,  Plana,  Bostroem  and 


INFECTION  207 

Others  have  found  it  on  the  awns  of  corn  which  were  imbedded 
in  the  tonsils  of  pigs  and  in  the  tongues  of  cattle.  Mayo 
states,  after  making  a  careful  study  of  this  disease,  that  the 
actinomyces  are  probably  a  degenerate  form  of  some  fungus 
which  grows  naturally  upon  food  stuffs  or  grain.  Bostroem 
entertains  the  view  that  they  develop  exclusiveh'  on  grain, 
particularly  on  the  awns  of  barley. 

§  164.  Infection.  While  actinomycosis  is  an  infectious 
disease  it  does  not  seem  to  be  transmitted  directly  from  one 
animal  to  another.  Numerous  investigators  have  tried  to  pro- 
duce the  disease  by  inoculating  cattle,  calves,  sheep,  goats, 
pigs,  dogs,  cats,  rabbits  and  guinea-pigs  with  actinomycotic 
lesions.  The  results  have  almost  invariably  been  negative 
when  pus  was  used,  but  the  disease  has  developed  after  inocu- 
lating cattle  with  pieces  of  tissue  containing  the  fungus  in  its 
vegetating  state. 

It  is  believed  that  the  infection  occurs  in  susceptible 
species  by  the  introduction  of  the  fungus  on  food  stuffs.  The 
supposition  is  that  the  parasite  gains  entrance  to  the  living 
tissues  through  slight  wounds  of  the  mucous  membrane  of  the 
mouth  or  throat  and  perhaps  the  alveoli  of  diseased  teeth  or 
during  the  shedding  of  the  milk  teeth.  It  multiplies  and  ex- 
tends from  the  points  of  entrance.  After  the  infected  awns 
once  gain  lodgement,  especiall}'  between  the  teeth,  they  are 
removed  only  with  difficulty.  The  favorite  points  for  the  act- 
inomyces to  enter  the  tongue  is  on  the  upper  surface  midway 
between  the  dorsum  and  the  tip.  The  lungs  may  be  the  seat 
of  primary  infection  due  to  the  inhalation  of  the  fungus.  The 
disease  has  been  rarel}-  observed  primarily  in  the  udder  but 
frequently  in  the  subcutaneous  tissue  about  the  head.  In 
man  the  source  of  infection  is  more  obscure.  Many  cases  have 
been  reported  where  the  individuals  did  not  come  in  contact 
with  diseased  animals  and  who  were  not  occupied  in  agricul- 
tural pursuits  or  in  handling  grain  but  who  were  glaziers, 
tailors  and  various  shop  tenders.  There  are  a  few  cases 
reported,  however,  where  the  circumstantial  evidence  points  to 
direct  infection  from  diseased  animals. 

The  present  knowledge  of  this  fungus  indicates  that    it 


2o8  ACTINOMYCOSIS 

must  attain  to  a  certain  stage  or  period  in  its  development 
before  it  will  live  and  multiply  in  living  animal  tissues.  It 
has  been  observed  that,  as  a  rule,  cattle  become  infected  when 
they  are  kept  upon  dry  food. 

§  165.  Symptoms.  Actinomycosis  is  manifested  by  a 
firm  swelling  or  tumor  usually  situated  in  the  region  of  the 
head  or  throat.  It  is  first  recognized  as  a  slight  swelling  of 
the  affected  part  resembling  somewhat  the  result  of  a  bruise. 
It  is  stated  by  those  wdio  have  had  much  experience  with  the 
disease  that  many  cases  of  actinomycosis  seem  to  be  caused  by 
blows  or  injuries  received  while  struggling  in  stanchions.  The 
enlargement  gradually  increases  in  size  and  ordinarily  it  is 
well  defined  from  the  surrounding  tissues. 

Upon  manipulation  the  tumor  feels  hard  and  dense  and  if 
it  is  not  the  result  of  the  bulging  of  the  adjacent  bone  it  is 
usually  attached  to  it.  In  the  region  of  the  throat  it  may  be 
fluctuating.  After  a  variable  length  of  time,  the  tumor  may 
soften  in  one  or  more  places,  rupture  and  discharge  a  rather 
thick,  yellowish  and  more  or  less  sticky,  purulent  substance. 
The  discharge  may  continue  or,  as  often  happens,  the  opening 
heals  temporarily  only  to  discharge  again.  The  discharge  often 
takes  place  into  the  cavity  of  the  mouth  or  throat.  Sometimes 
the  neoplastic  tissue  increases  in  amount  until  it  gradually 
forces  its  way  through  the  opening  resembling  somewhat  a 
cauliflower  in  appearance.  The  actinomycotic  growth  fre- 
quently increases  rapidly  in  size  after  it  has  discharged.  In 
later  stages  the  teeth  may  become  ulcerated  and  loose. 

When  the  tongue  is  affected  the  animal  finds  it  difficult  to 
eat.  The  organ  is  swollen  and  in  advanced  cases  hangs  from 
the  mouth  with  abundant  salivation.  When  the  pharynx  is 
affected  there  is  difficulty  in  swallowing  and  when  the  larynx 
is  attacked  there  is  difficulty  in  breathing.  In  this  countr}^ 
the  tumor  is  most  frequently  seen  on  the  external  surface  of 
the  jaw.  It  is  stated  by  Salmon  that  it  usually  begins  in  the 
connective  tissue  beneath  the  skin  but  soon  extends  to  the  bone 
which  it  penetrates.  Actinomycosis  of  the  cervical  vertebrae 
may  cause  spinal  paralysis.  When  the  lungs  are  attacked  the 
animal  may  present  the  appearance  of  one  suffering  from  a 
chronic  pulmonary  disease  such  as  tuberculosis. 


MORBID    ANATOMY  209 

Actinomycosis  is  not  a  rapidly  fatal  disease.  Animals 
rarely  if  ever  die  from  its  immediate  effects.  The  length  of 
time  during  which  they  survive  depends  very  largely  upon  the 
location  of  the  tumor  and  the  rapidity  of  its  development.  If 
the  tumor  is  situated  where  it  does  not  interfere  seriously  with 
prehension,  mastication  or  swallowing  of  food  or  w^here  it 
does  not  occlude  or  press  upon  the  respiratory  passages  the 
animal  usually  survives  for  several  years.  When  death  occurs 
it  is  usually  due  to  inanition,  the  animal  being  unable  to  take 
sufficient  food,  although  the  drain  upon  the  system  by  the 
long  continued  discharge  of  pus  must  be  severe.  Mayo 
reports  several  cases  where  the  disease  was  watched  for  five  or 
six  years  and  where  it  would  probably  have  continued  several 
years  more  had  the  animals  not  been  destroyed.  Most  animals 
which  become  affected  with  actinomycosis  are  either  destroyed, 
treated  or  slaughtered  for  beef  in  the  early  stages  of  the 
disease. 

§  166.  Morbid  anatomy.  The  actinomycotic  tumors 
have  in  or  near  their  centers  rosettes  of  the  ray  fungus 
surrounded  by  cells.  The  newly  formed  tissue  consists  princi- 
pally of  epithelioid  and  spindle  shaped,  connective  tissue  cells, 
among  which  giant  cells  may  appear.  As  these  cells  increase 
in  number  they  press  against  the  surrounding  tissues  produc- 
ing the  hard  and  dense  tumors.  This  is  especially  true  when 
they  are  located  in  the  connective  tissue.  In  certain  other 
positions,  such  as  the  liver,  the  inflammatory  cells  are  sur- 
rounded by  a  fibrous  tissue  framework  which  gives  to  the 
lesion  a  honey  comb  appearance.  On  section  a  disagreeable 
"nutty"  odor  is  given  off  which  Mayo  considers  to  be  quite 
characteristic  of  the  disease.  The  outside  of  the  tumor  is 
usualh^  composed  of  a  dense  layer  of  fibrous  connective  tissue. 
Extending  from  the  periphery  toward  the  center,  the  tissue 
becomes  less  dense  and  is  composed  largely  of  epithelioid  cells. 
In  the  softer  tissue  there  are  often  cavities  of  greater  or  less 
size  filled  with  a  viscid,  purulent  substance  in  which  the  small, 
yellowish  granules  of  the  ray  fungus  can  be  found.  If  this 
pus  is  spread  in  a  thin  layer  on  a  smooth  surface  granules 
composed  of  this  fungus   growth    can  often  be  seen  with   the 


2IO  ACTINOMYCOSIS 

unaided  eye.  These  pus  cavities  are  usually  connected  with 
each  other  by  small  sinusts  but  sometimes  they  are  separated 
bv  bands  of  fibrous  tissue. 


Fig.  45.     Head  of  a   steer  with   actinomycosis   of  the  lower  jaw. 
{Photographed  by  Hopkins. ) 

If  the  disease  is  in  the  bone,  usually  in  the  head,  as  it  is 
where  the  specific  organism  gains  entrance  and  begins  to  grow 
in  the  interior  of  the  bone,  the  bone  tissue  about  the  organism 
becomes  in  places  disintegrated  and  absorbed  and  pockets  are 
formed  containing  the  fungus.  While  the  interior  of  the  bone 
is  being  broken  down  and  absorbed  by  the  action  of  the  acti- 
nomycotic growth  within,  its  diameter  is  being  increased  by 
the  deposition  of  new  tissue  until  it  may  become  several  times 
its  normal  size. 

The  disease  spreads  within  the  body  in  most  cases  by 
gradual  invasion  of  the  tissues  surrounding  the  infected  point. 
At  the  seat  of  infection,  minute,  inflammatory  points  appear 
which  extend  at  their  periphery  and  unite  to  form  larger  areas 
of  diseased  tissue.  These  masses  tend  to  extend  in  one  direc- 
tion and  to  heal  in  another  leaving  behind  bands  of  cicatricial 


MORBID    ANATOMY 


21  I 


tissue.  The  process  usually  differs  widely  from  that  of  a 
simple  inflammation.  In  its  progress  the  disease  shows  no 
preference  for  structures  but  invades  one  tissue  after  another 
so  that  all  may  be  involved  alike. 

The  lymphatics  show  no  constant  tendency  to  become 
involved.  Metastasis  occurs  in  a  very  small  proportion  of  the 
cases.  When  it  does,  as  reported  by  Ponfick,  large  areas  may 
be  simultaneously  affected.  He  reports  a  case  in  the  human 
subject  in  which  the  left  jugular  vein  was  perforated  by  a  mass 
of  the  fungi  resulting  in  the  formation  of  actinomycotic  infarcts 
in  the  lungs,  spleen,  brain,  and  heart. 

In  cattle,  actinomycosis  usually  appears  in  one  or  more  of 
the  following  locations,  viz.:  (i)  in  the  maxillary  bones  it 
generally  results  in  large  tumors.  Actinomycosis  of  the 
jaw  usually  commences  with  flat  granulations  of  the 
sums    and    mucous    membranes   in  the  neighborhood    of    the 


Fig.   46.      Photograph   of  a  section  through  an  actinomycotic  jaw. 
(a)  tooth,  [b]  bone,   [c)  actinomycotic  tissue. 

teeth  and  spreads  finally  to  the  medullary  tissues  of  the  bone 
and  to  the  periosteum  soon  giving  rise  to  the  osseous  tumor. 
From  the  maxillary  bone  the  disease  may  advance  either  to 


212 


ACTINOMYCOSIS 


the  subcutaneous  connective  tissue  and  the  skin  or  to  the  oral 
cavity  in  the  direction  of  the  molar  teeth  which  become  dis- 
placed. (2)  In  the  tongue.  When  the  disease  appears  in  this 
organ  it  takes  the  form  of  an  indurating  glossitis.  The  tongue 
becomes  thicklj'  sprinkled  with  round  or  oval,  hard,  fibrous 
nodules  which  finally  become  purulent  or  chalky  at  the  center. 
Around  these  there  is  a  con.siderable  increase  of  connective 
tissue  which  leads  to  the  atrophy  of  the  mu.scle  fibers,  l^pon 
.section  the  tongue  is  found  to  be  hard  and  often  gritty.  The 
indurated  tongue  is  often  eroded   from    friction    and   various 


Fig.  47.     Actinomycosis  of  the  Jaw.     {Photographed  by  Hopkins.') 

deformities  of  this  organ  are  reported.  (3)  In  the  pharynx 
the  disease  usuall}-  takes  the  form  of  soft  polypoid  or  fungoid 
nodules  or  lumps  with  a  smooth  surface  and  short  peduncle. 
These  nodules  vary  in  size  often  reaching  that  of  a  goose's 
^Zg.  The.se  polypoid  growths  may  cause  great  difficulty  in 
swallowing  and  likewise  interfere  with  respiration.  Tumors 
of  this  kind  may  form  in  the  oesophagus  or  trachea.  Rarely 
actinomycotic  growths  occur  at  other  places  in  the  alimentary 
tract.       There    are    some    cases    in    which    the    lesions    are 


MORBID    ANATOMY  213 

not  restricted  to  the  digestive  tract.  (4)  In  the  skin  and  sub- 
cutaneous tissue  the  lesions  are  found  chiefly  on  the  head  and 
neck.  They  usually  consist  of  firm  nodules  from  the  size  of  a 
hazel  nut  to  that  of  a  man's  fist  or  even  larger.  Sometimes 
these  nodules  are  pedunculated  and  at  others  they  are  attached 
to  the  skin  by  a  broad  base.  Instead  of  the  hard  tumor  there 
may  occur  soft  granular  fungoid  proliferations  covered  with  a 
brown  crust  or  with  a  purulent  secretion.  At  other  times 
minute  nodules  appear  in  these  proliferations  and  the  skin 
becomes  thickened  and  indurated.      However,  the  skin  lesions 


Fig  48.     u^ciitiouiycosis  of  the  tongue,  ''ivoodcn  longue.''     {Photo- 
graphed by  Hopkins.) 

may  become  very  large.  In  this  organ,  the  disease  may  be 
either  primary  or  secondary.  (5)  In  the  lymph  glands 
actinomycosis  often  appears  in  the  lymph  glands  of  the  head, 
larynx  and  pharynx.  The  parotid  and  submaxillary  glands 
are  sometimes  involved  as  secondary  infections.  It  is  reported 
that  the  sub-parotid  glands  are  most  frequently  affected. 
(6)  In  the  lungs  the  lesions  vary.  They  may  consist  of  firm, 
somewhat  yellowish  nodules  which  eventually  become  cal- 
careous in  their  center  and  vary  in  size  from  mere  specks 
to  that  of  a  pea.  This  form  is  spoken  of  as  miliary  actinomy- 
cosis.     In   the  second  form  the  actinomycotic  foci  soften  and 


214  ACTINOMYCOSIS 

become  filled  with  a  gray  miico-purulent  fluid.  The  lesion 
may  spread  to  the  pleurae  and  even  reach  to  the  surface  of 
the  body  by  penetrating  through  the  thoracic  wall.  The 
bronchial  glands  and  the  mucosa  of  the  air  passages  may 
also  become  affected.  (7)  Actinomycosis  has  been  reported 
rarely  as  attacking  the  udder,  spermatic  cord,  brain,  spleen, 
liver,  muscle,  diaphragm,  peritoneum,  inguinal  glands,  vagina, 
uterus  and  cervical  vertebrae. 

It  is  stated  by  Salmon  that  in  England  the  disease  appears 
mo.st  often  in  the  tongue,  in  Denmark  the  .soft  parts  of  the 
head  are  affected  most  frequently  while  in  some  parts  of 
Germany  it  is  most  frequently  found  in  the  pharynx.  In  the 
United  States  it  usually  appears  in  the  lower  jaw.  In  man, 
as  already  stated,  actinomycosis  rarely  occurs.  Here,  as  in 
cattle,  the  appearance  of  the  lesions  vary  according  to  the 
nature  of  the  part  affected.  In  some  cases  the  lesions 
closely  resemble  those  of  chronic  inflammation  but  in  others 
such  as  the  liver  or  skin  they  are  often  characteristic.  In  the 
lungs  the  lesions  have  frequently  been  mistaken  for  tubercle. 
Usually  the  disease  affects  the  head  and  if  the  maxillary  bones 
are  attacked  the  teeth  are  usually  lost. 

Actinomycosis  i)i  scciue.  Actinomycosis  appears  in  this 
species  in  the  lower  jaw,  larynx,  lungs,  wounds  caused  by 
castration,  in  the  mammar}-  gland,  muscle  and  b'ones.  The 
character  of  the  lesions  does  not  differ  to  any  marked  extent  in 
swine  from  those  in  cattle  or  man.  In  case  of  bone  infection 
purulent  cavities  and  sinuses  are  formed  in  which  the  yellow 
granules  of  the  fungus  occur.  It  is  reported  that  occasionally 
the  pig  suffers  from  generalized  actinomycosis.  Duncker  has 
found  in  the  muscles  of  the  pig  a  variety  of  the  ray  fungus 
which  has  been  called  Actijioviyces  miiscoloruvi  siiis,  to  dis- 
tinguish it  if  possible  from  the  bovine  species.  Its  relation 
to  the  actinomyces  bovis  has  not  been  clearly  determined.  It 
is  reported  to  have  been  found  frequently. 

Actinomycosis  in  Iiorscs  and  sheep.  In  the  horse,  acti- 
nomycosis of  the  bones,  tongue,  trachea,  spermatic  cord  and 
submaxillary  glands  has  been  ob.served.  The  disease  is 
reported  to  have  been  mistaken   for  glanders.     The   affection 


DIFFERENTIAL    DIAGNOSIS  215 

known  as  scirrhous  cord  seems  to  be  due  in  rare  cases  to  an 
infection  by  the  ray  fungus.  One  such  case  has  occurred  in  the 
clinic  of  this  institution.  A  very  few  ca.ses  of  this  disease 
have  been  reported  in  sheep  the  lesions  being  restricted  to  the 
lungs  or  muscles. 

§  167.  Differential  diagnosis.  In  cattle  actinomycosis 
is  to  be  differentiated  (i)  from  tuberculosis,  especiall}'  of  the 
lungs,  glands  about  the  throat,  head  and  the  udder,  (2)  vari- 
ous forms  of  glossitis,  polypoid,  growths  in  the  pharynx, 
fibroma,  sarcoma  and  osteosarcoma  of  the  jaw,  parotitis  and 
•cellulitis.  The  writer  has  seen  a  few  cases  of  bacterial  infec- 
tion of  the  maxillary  glands  giving  rise  to  the  formation  of 
large  quantities  of  caseous  matter  which  caused  swelling  and 
firmness  suggestive  of  actinomycotic  tumors.  In  one  instance 
a  specimen  reported  to  be  actinomycosis  was  examined  and 
found  to  contain  a  piece  of  bone  about  three  inches  long  which 
bad  become  wedged  between  the  teeth  and  cheek  and  sur- 
rounded by  infiammator}'  tissues.  Frohner  calls  attention  to 
contagious  pleuro-pneumonia  and  foot  and  mouth  disease  as 
possibly  being  mistaken  for  this  disease. 

In  making  a  positive  diagnosis  of  actinomycosis  it  is 
necessary  to  make  a  microscopic  examination  of  some  of  the 
■diseased  tissue  or  of  the  discharged  pus  in  which  the  ray 
fungus  may  be  found  if  the  disease  is  actinomycosis.  It  is 
impossible  to  obtain  this  positive  proof  from  the  living  animal 
when  the  disease  is  situated  in  the  internal  organs.  With 
these  it  is  necessar}-  to  depend  largeh'  upon  the  history  and 
general  condition  of  the  animal.  In  preparing  the  discharged 
pus  for  a  microscopic  examination  it  is  usuall}'  sufficient  to 
crush  one  or  more  of  the  yellowish  granules  between  a  slide 
and  cover-glass.  It  is  of  advantage  to  wash  it  with  a  dilute 
solution  of  caustic  soda  to  clear  awa}'  the  pus  cells.  The  ro- 
setts  are  easily  recognized  with  a  low  magnification. 

In  man,  actinomycosis  is  to  be  differentiated  from  certain 
forms  of  tuberculosis  and  the  Madura  foot  disease  which  was 
described  by  Carter,  in  i860,  as  a  "fungous  disease."  This 
is  a  chronic,  locally  spreading  inflammation  of  the  foot,  rarely 
•of  the  hand,  causing  the  destruction  of  the  part  involved  and 


2l6  ACTINOMYCOSIS 

giving  rise  to  a  great  overgrowth  of  connective  tissue.  M}'- 
cetoma  almost  invariably  attacks  the  hand  or  foot  and  accord- 
ing to  Carter  there  are  no  secondary  deposits  in  the  viscera. 
In  actinomycosis  the  extremities  are  rarely  attacked  and  the 
viscera  are  often  the  seat  of  the.  disease  ;  further  the  mycetoma 
is  a  disease  of  hot  climates  while  actinomycosis  is  a  disease  of 
the  temperate  latitudes.  The  fungus  of  the  two  affections 
seem  to  be  closely  related  but  as  yet  their  identity  has  not 
been  established. 

§  i68.  Specific  treatment.  The  investigations  of  Thomas- 
sen,  Nocard,  and  Norgaard  and  the  trials  of  a  large  number  of 
veterinarians  have  proved  very  conclusively  the  specific,  cura- 
tive effect  of  iodide  of  potassium.  According  to  Salmon  the 
iodide  of  potassium  is  given  in  doses  of  from  i%  to  2^2  drams 
dissolved  in  water  and  administered  in  a  drench,  once  a  day. 
The  dose  should  var}-  somewhat  with  the  size  of  the  animal 
and  with  the  effects  that  are  produced.  If  the  dose  is  suffi- 
ciently large  there  appear  signs  of  iodism  in  the  course  of  a 
week  or  ten  days.  The  skin  becomes  scurfy,  the  eyes  mois- 
tened, nasal  catarrh  and  loss  of  appetite.  When  these  symp- 
toms appear  the  medicine  may  be  suspended  for  a  few  days 
and  afterwards  resumed  in  the  same  dose.  The  cure  requires 
from  three  to  six  weeks  treatment.  Some  animals  do  not  im- 
prove with  the  administration  of  iodide  of  potassium  and 
these  are  generally  the  ones  which  show  no  signs  of  iodism. 

If  there  is  no  sign  of  improvement  after  the  animals  have 
been  treated  four  or  five  weeks  and  the  medicine  has  been 
given  in  as  large  doses  as  appear  desirable,  it  is  an  indication 
that  the  particular  animal  is  not  susceptible  to  the  curative 
effects  of  the  drug  and  the  treatment  should  be  abandoned. 

It  is  not,  however,  advisable  to  administer  iodide  of  potas- 
sium to  milch  cows,  as  it  will  considerably  reduce  the  milk 
secretion  or  stop  it  altogether.  Furthermore,  a  great  part  of 
the  drug  is  excreted  through  the  milk  making  it  unfit  for  use. 
It  should  not  be  given  to  animals  in  advanced  pregnancy,  as 
there  is  danger  of  producing  abortion. 

§  169.  Sanitary  considerations.  The  literature  upon 
this  subject  is  largely  to  the  effect  that  actinomycosis  is  rarely 


SANITARY    SIGNIFICANCE  21J 

if  ever  either  contagious  or  infectious  in  the  sense  that  it  can  be 
transmitted  from  one  animal  to  another  or  from  one  of  the 
lower  animals  to  man.  There  seems  to  be  no  indisputable 
case  on  record  of  such  a  transmission  although  a  few  cases  are 
very  suggestive.  It  is  the  opinion  of  most  pathologists  that 
when  the  disease  is  restricted  to  small  tumors  and  these  are 
localized,  that  the  affected  parts  should  be  destroyed  but  the 
remainder  of  the  carcass  may  be  used  for  human  consumption. 
In  Bulletin  No.  2,  of  the  Board  of  L,ive  Stock  Com- 
missioners of  Illinois,  published  in  1891  is  the  report  of  the 
somewhat  famous  trial  in  the  Peoria  county  circuit  court  of  the 
case  of  J.  B.  Greenhut  et  a/,  vs.  John  M.  Pearson  ef  al.  to  re- 
cover damages  for  the  rejection  and  destruction  of  certain 
actinomycotic  cattle,  in  which  is  given  the  testimony  of  a  large 
number  of  distinguished  veterinarians  and  sanitarians  concern- 
ing the  wholesomeness  of  the  meat  of  cattle  affected  with  this 
disease.  Although  at  that  time  there  was  a  strong  popular 
sentiment  against  the  use  of  such  animals,  the  jury  after  a 
forty  hours'  consideration  reported  their  inabilitv  to  agree  and 
were  discharged  by  the  court.  The  most  conspicuous  feature 
of  this  evidence  was  the  inability  of  the  witnesses  to  produce 
satisfactory  evidence  of  the  communicability  of  the  disease 
from  animal  to  man.  This  evidence  did  much  to  show  that 
the  danger  from  this  disease  in  eating  meat  of  affected  animals 
was  after  all  a  matter  of  opinion,  fear  or  sentiment  rather  than 
a  demonstrated  fact.  Mayo,  in  his  bulletin  upon  the  subject, 
states  that  there  is  no  danger  of  persons  contracting  this  dis- 
ease from  eating  the  flesh  of  affected  animals  provided  the 
visibly  diseased  portions  are  removed. 

REFERENCES. 

1.  BOSTROEM.  Untersuchungen  iiber  des  Aktinomykose  des  Men- 
schen.  Beitrag.  zur  path.  Anat.  11.  ziir  allgr.  Pathologic.  Bd.  IX. 
(1S91)  S.  I. 

2.  Israel.  Neue  Beobachtungen  auf  dun  Gebeite  des  Mvkosen 
des  Menschen.      Virchou^s  Archives.    Bd.  LXXVI.     (1878)8.11! 

3.  M.w'o.  Actinomycosis  bovis  or  "lump)' -jaw."  Bulletin  No.  j8^ 
Kansas  State  Agric.  Exp.  Station.     1S92. 

4.  NocARD.  Notes  sur  ractinomycose  des  animaux.  Recueil  de 
Med.  Veter.     Vol.  LXIX.    (1892)  p.  167. 


2l8  LEECHES 

5.  Salmon.     Treatment  of  lumpy -jaw  or  actinomycosis  in  cattle. 
Bidletin  No.  2,  U.  S.  Bureau  of  Annual  hidnstry.     1893. 

6.  Salmon.    Actinomj-cosis  or  lumpy-jaw.    Annual  Report,  Bureau 
of  Animal  hid uslrv.     1893-4,  p.  88. 

7.  Wolff  and   Isr.a.EL.     Ueber  Reincultur  des  Actinomyces  und 
seine  Uebertragbarkeit  auf  Thiere.  Vireh.  Arch.    Bd.  XXVI.  (1891J  S.  11. 


LEECHES. 


§170.  Characterization.  "Leeches"  or  "Leeching" 
is  an  infectious  disease  quite  prevalent  among  the  horse  kind 
in  Florida  with  lesions  localized  on  the  skin  or  the  mucosa  of 
the  head.  It  is  thought  by  many  that  this  affection  is  identical 
with  the  disease  known  as  bursattee*  in  India. 

This  disease  is  known  by  a  variety  of  names  such  as  : 
barsati,  barsati,' barsattee,  barsatti,  bausette,  bursati,  bursatie, 
bursatti.  bursautee,  bursautie,  bursauttie,  bursottee,  burusatee 
and  burusauttee.  These  names  have  been  derived  from  the 
Indian  word  burns  or  bursat,  meaning  rain  or  rain  sore,  it 
having  been  supposed  that  the  malady  was  associated  with  the 
rain}'  season. 

Dr.  L.  C.  Neal.  of  Florida,  described  it  as  affecting  horses 
and  cattle.  He  believes  it  to  be  peculiar  to  that  section,  where 
he  states,  it  is  common  and  very  fatal  to  horses  and  mules. 
There  are  hundreds  of  ponds  in  the  central  portion  of  the 
state  around  the  margins  of  which  there  is  usually  a  belt  of 
gra.s.S5'  prairie,  water  grass  and  water  lilies.  Into  these  grass}' 
places  the  horses,  mules  and  cows  often  go  during  the  summer 
and  feed  all  da}-  in  the  water.  He  adds,  "after  a  varying 
exposure  to  the  influence,  or  whatever  it  ma}-  be  called,  of  the 
'pond,'  a  slight  lump  or  elevation  of  the  skin  ma}-  be  found  on 
some  part  of  the  body  that  has  been  submerged.  To  the  touch 
it  will  feel  as  if  a  grain  of  shot  were  lodged  beneath  the  skin. 
In  eight  or  ten  days  the  skin  sloughs  off  centrally  over  this 
hard  spot,  leaving  a  blood}',  bruised-like  surface.     This  rapidly 


*It  seems  to  be  true  that  an  entirely  different  affection  is  known  by 
the  same  name  in  the  northern  portion  of  the  United  States.  The  term 
"  Leeches  "  is  also  applied  to  the  condition  following  the  invasion  of  the 
liver  fluke  {Fasciola  hepatica). 


CHARACTERIZATION  219 

grows  in  size  till  in  a  few  weeks  there  is  a  raw  surface  from  4 
inches  to  a  foot  square.  This  oozes  blood  and  serum,  but  no 
pus.  An  examination  will  show  usually  a  mass  of  yellow,  gritty 
growth,  coral  like  in  shape,  embedded  in  a  mass  of  bruised, 
bloody  tissue,  dark  in  color  and  the  edges  roughened,  elevated 
above  the  skin,  and  the  .skin  decaying  at  the  outside  of  the  ulcer. 
The  leech  invades  most  any  tissue,  but  seems  most  common 
on  the  legs,  abdomen,  and  sides.  Occasionally  it  is  found  in 
the  head.  The  invaded  tissues  decay  slowly  and  apparently 
without  pain.  I  have  seen  hoofs  cut  off,  the  abdomen  opened, 
the  eyes  eaten  out  and  the  teeth  destroyed." 

In  this  country  the  disease  has  not  attracted  very  much 
attention,  nor  has  it  been  considered  of  much  economic 
importance.  An  explanation  for  this  may  be  offered  on  account 
of  its  seemingly  noncontagious  character  and  that  it  has  been 
thought  to  be  confined  to  comparatively  limited  areas,  and  that 
the  animals,  although  infected,  may  yet  be  utilized  for  some 
purposes.  On  account  of  the  chronic  course  of  the  disease 
the  affected  animals  from  a  sentiment  of  mercy  are  often  killed 
before  the  disease  can  terminate  fatally. 

Although  this  affection  presents  many  points  of  similarity 
to  the  one  found  in  India,  the  question  of  their  complete 
identity  ought  to  be  held  in  abeyance  until  a  more  thorough 
investigation  can  be  made. 

In  a  recent  publication,  Dawson,  of  the  Florida  Experi- 
ment Station,  states  "that  'leeches'  or  bursattee  is  a  common 
disease  in  Florida,  which  manife.sts  itself  in  the  formation  of 
tumor-growths  which  have  some  of  the  characters  of  actinomy- 
cotic tumors.  Its  structure  is  fibrous,  and  contains  many  sin- 
uses, which  discharge  a  bloody,  honey-like  fluid.  It  is  a 
fatal,  infectious  disease,  which  has  its  origin  in  the  skin  and 
finally  penetrates  all  the  tissues.  Here  and  there  in  the 
tumor  tissue  yellow  bodies  with  root  like  projections  may  be 
found.  These  bodies  are  called  '  leeches  '  by  the  natives. 
They  consi.st  of  the  mycelia  of  the  fungus  which  causes  the 
disease.  The  only  remedy  is  the  complete  removal  of  the 
tumor  and  adjacent  tissue  at  once.  The  application  of  caus- 
tics and  disinfectants  make  matters  infinitely  worse,  as  they 


2  20  LEECHES 

Stimulate  the  tissues  to  renewed  growth-activit}-.  In  Florida 
the  disease  affects  only  the  genus  equus." 

§  171.  History.  lu  1896,  some  of  the  diseased  tissue 
from  cases  of  this  affection,  in  Florida,  were  sent  to  the 
Bureau  of  Animal  Industr}'  for  investigation.  They  were 
studied  by  Dr.  P.  A.  Fish  who  made  an  extended  report  on 
the  results  of  his  findings.  He  also  gave  a  very  complete 
review  of  the  literature. 

A  summary  of  the  literature  shows  that  among  the  old 
theories  "Leeches"  was  believed  to  be  a  blood  disease  in  many 
ways  not  unlike  syphilis,  scrofula  and  farcy.  The  "fly 
theory"  of  the  causation  and  dissemination  of  bursattee  was 
entertained  by  the  natives  of  India  as  early  as  1820.  Jackson, 
in  1842,  seems  to  have  been  the  first  to  believe  that  there  was 
any  connection  between  the  disease  and  a  fungus. 

Hodgson,  in  1853,  referred  to  the  sores  as  cancerous  ulcers 
and  Hart  in  1872,  was  strongh'  inclined  to  pronounce  it 
cancer,  although  he  could  not  confirm  this  view  structurally 
by  microscopic  examination  of  the  tissue.  It  seems  to  be 
generally  accepted  that  the  disease  is  peculiar  to  the  Tropics, 
but  cases  have  been  reported  in  Kansas  and  Minnesota  in  the 
United  States,  not  only  during  the  summer  months,  but  when 
the  thermometer  registered  below  zero.  We  might  also  expect 
that  the  disease  would  exist  in  Mexico  and  Central  and  South 
American  countries,  where  the  conditions  of  temperature  and 
moisture  are  favorable. 

Reports  show  that  a  high  temperature  is  essential  for  the 
development  of  the  disease,  although  exceptional  cases  are 
noted  as  occurring  during  the  cold  season.  Moisture  does  not 
seem  to  be  necessary,  since  many  cases  develop  when  the 
season  is  dry.  It  is,  however,  an  important  factor.  Statistics 
show  that  cases  are  more  numerous  and  that  the  disease 
assumes  a  more  aggravated  form  during  the  wet  season. 

In  India,  native  as  well  as  foreign  bred  horses  are  sus- 
ceptible, but  according  to  some  writers,  none  of  the  other 
equine  species  are  affected. 

In  the  United  States  mules  and  cattle  are  said  to  develop 
it,  but  not  as  readily  as  the  horse.    Outbreaks  among  cattle  are 


GEOGRAPHICAL    DISTRIBUTIOX  22  1 

comparatively  rare.  Thin-skinned  animals  are  more  susceptible 
than  thick-skinned  ones.  Some  discrepancy  of  opinion  exists 
as  to  the  kind  of  horses  most  likely  to  take  the  disea.se  (assum- 
ing that  bursattee  and  leeches  are  similar).  Xeal  states  that 
only  horses  of  good  blood  leech,  and  the  Cuban  and  Texan 
ponies  are  as  a  rule  exempt.  Anderson  states  that  it  is  the 
coarsely  bred  and  hard-worked  horses  that  are  the  most  sus- 
ceptible. The  well-bred  ones,  having  the  advantage  of  good 
hygienic  surroundings,  rarely  contract  it. 

§  172.  Geographical  distribution.  Bursattee  has  been 
reported  from  Burmah«and  Hindoostan.  It  is  thought  that  the 
prevalence  of  the  di.sease  is  associated  with  the  principal  river 
systems  of  India.  In  the  hilly,  rocky  and  consequently  drier 
districts  there  is  a  very  noticeable  diminution  or  absence  of  it. 

Outside  of  India  there  seems  to  have  been  no  cases  of  this 
malady  reported  except  in  the  United  States,  unless  upon  fur- 
ther investigation  certain  mycotic  diseases,  which  have  been 
described  in  Europe,  should  prove  to  be  identical  with  it. 

Lyford  (1866)  reported  it  in  Minnesota,  Anderson  (1889) 
in  Kansas  and  Alabama,  and  Neal  (1887)  and  Bitting  (1894) 
in  Florida.  The  latter  writer  states,  that  it  is  "now  known 
all  over  the  United  States  except  in  that  region  lying  east  of 
Alleg-liany  mountains  and  north  of  the  Potomac  river. "  A  few 
cases  have  been  presented  for  treatment  in  the  clinic  of  the 
New  York  State  A'eterinar}-  College. 

§  173.  Etiology.  Jackson  suggested,  in  1S42,  that  the 
di.sease  might  be  related  to  a  fungus  or  to  a  vegetable  parasite. 
Collins,  in  1874,  expressed  a  similar  belief.  F.  Smith,  in  1879 
and  1884,  seems  to  have  been  the  first  to  have  worked  along 
this  line.  He  was  able  to  find  fungi  in  every  fresh  specimen 
of  the  sores  that  he  examined.  Steel,  in  1881,  also  found 
fungal  elements  in  these  sores.  T.  Smith,  in  1S93,  examined 
some  alcoholic  material  and  gave  expression  to  the  belief  that 
the  disease  was  caused  by  a  fungus.  Fish,  in  1896,  found  a 
fungus  embedded  in  the  diseased  tissue.  He  did  not  name  it 
neither  did  he  obtain  it  in  pure  culture,  but  his  illustrations 
are  very  clear  in  showing  the  existence  of  a  fungus.  Fish 
gives  in  detail  the  methods  he  employed.      It  is  to  his  work 


222  LEECHES 

that  we  are  indebted  for  the  more  careful  description  of  the 
morbid  changes. 

§  174.       Morbid     anatomy.  ^ 

As  a  rule  the  lesions  are  near  the  r  1&^** 

surface.  Where  the  diseased 
portion  has  become  well  devel- 
oped there  is  usually  a  more  or 
less  complete  detachment  of  the 
central  inflammatory  growth  from 
the  surrounding  tissue.  This  v^o.  a<^.  A  piece  cut  from  the 
nodular  or  '  'kunkur' '  growth  ma}-  Up  ofati  affected  horse,  showing 
vary  in  its  density    according    to   several  diseased  foci.      (Some- 

,1  .  r     -i.  '     J        1  i      what  reduced.)     (Fish.) 

the    stage    of    its     development.  '    ^ 

During  the  earlier  stages  it  is  soft  and  easily  cut  ;  later  it  be- 
comes firmer  and  ultimately  assumes  a  hard  or  "gritty" 
character. 

In  cutting  sections  it  is  generally  the  exception  to  cut 
through  the  nodule  or  kunkur  evenly  and  to  have  it  retain  its 
proper  relation  with  the  other  parts.  Even  if  successful  in 
cutting,  the  nodule  drops  out  during  some  of  the  later  proces- 
ses. In  the  specimens  examined  the  lesions  were  confined 
entireh'  to  the  skin  and  subcutaneous  tissue  ;  no  traces  of 
muscular  or  glandular  structure  were  observed.  iVround  the 
central  portion  of  the  inflammatory  growth  there  is  a  zone  of 
leucocytes  of  the  mononuclear  and  polynuclear  varieties,  the 
latter  predominating.  They  are  embedded  in  an  abundant 
stroma  of  connective  tissue  which  is  in  a  greater  or  less  stage 
of  degeneration.  The  central  portion  of  the  zone  is  in  some 
cases  very  closely  packed  with  the  leucocytes,  while  toward 
the  periphery  the}'  are  more  loosely  arranged  and  cause  a 
marked  irregularity  of  the  margin  from  their  uneven  drifting 
into  the  tissue  beyond.  There  is  geueralh^  one  and  perhaps 
more  points  where  this  infiltration  occurs  quite  extensively. 
In  some  of  the  preparations  the  wandering  cells  have  been 
traced  as  far  as  the  surface  of  the  epidermis. 

Occasionally  there  may  be  found  a  narrow  area  at  the  per- 
iphery of  the  nodule,  as  seen  in  cross  section,  which  is  lighter  in 


'i4i«|||j||l|^ 


MORBID    ANATOMY  223 

color  and  less  dense  in  texture  than  the  central  mass,  evidently 

an  extension  of  the  growth. 

In  the  specimens  examined 
the    parts     where     the     lesions 
abounded  were  not  characterized 
by  a  rich  vascular  supply.      The 
few   vessels   that    were    encoun- 
tered were  not  of  a  normal  char- 
acter ;    their    walls    were  thick- 
ened, and    the    endothelium,   in- 
FiG.  50.     From  the  same  lip,  stead     of    presenting    the    usual 
but  shocus  a  larger  infected  area,    flattened   appearance,  was  irreg- 
^^'^^^■)  ularly  cylindrical.    Although  the 

condition  was  not  observed,  it  is  not  impossible  that  the 
hyphae  of  the  fungus  may  develop  to  such  an  extent  as  to 
compress  or  actually  penetrate  the  walls  of  the  vessels,  caus- 
ing inflammatory  changes  sufficient  to  permit,  in  the  course  of 
time,  a  disorganization  or  absorption  of  a  portion  of  the  ves- 
sel itself,  and  that  ultimately  it  may  become  incorporated  in 
the  nodule. 

The  nodules  are  generally  irregularly  cone  shaped  and  are 
of  variable  size.  In  section  they  reveal  a  very  dense  structure, 
the  framework  of  which  forms  a  close  reticulum. 

Within  the  meshes  are  what  appear  to  be 
leucocytes  in  various  stages  of  disintegration, 
and  free  nuclei.  Among  these,  at  places, 
there  can  be  seen  small  bodies  of  nearly  the 


same  size  as  the  nuclei  and  taking  the  stains  Fig.  51.    An 

in  the  same  way,   but  differing  in  form.      At   isolated  nodule 
one  portion  of  its  circumference  the  substance  shoiving  the  char- 

of  the   body   is   seen   to   draw  itself  toward  a  ,  ,7., 

/  ened.,      coral-like 

point  and  in  favorable  preparations  that  point  appearance  of  the 
has  been  followed  some  little  distance  as  a  mass.  {Fish.) 
delicate  filament.  In  mo.st  cases  the  filament  remains  un- 
stained, or,  as  observed  in  a  Gram-eosin  preparation,  the  club 
end  may  stain  blue  and  the  filament  red.  Exceptionally  one 
may  find  a  clear  area  or  vacuole  in  one  of  the  clubs.  From 
the  fact  that  the  filament  is  not  usually  traceable  to  its  central 


224 


LEECHES 


connection  a  more  or  less  flagellate  appearance  is  given  to   the 
fungus,  which  represents  a  condition  not  believed  to  exist. 

Not  infrequently  small  spherical  bodies  are  found  not  far 
from  the  clubs  which  take  the  stain  readily  and  whose  size  is 
sufficiently  small  to  admit  of  the  possibility  of  their  being 
spores.  The  free  ends  of  many  of  the  clubs  point  toward  the 
periphery  of  the  nodule,  but  this  is  not  a  constant  feature. 

The  framework  of  the  nodule  stains  very  slightly  or  not 
at  all  and  .shows  among  the  enmeshed  corpuscles  as  a  very 
irregular,  distorted  and  somewhat  glistening  network.  It  is 
this  portion  of  the  nodule  that  gives  the  hard,  gritty  feeling, 
and  is  probably  due  to  a  greater  or  less  deposition  of  lime  salts 
along  the  reticulum.  It  appears  that  the  framework  of  the 
nodule  is  composed  of  a  mycelial  net,  which  in  the  course  of 
development  has  become  more  or  less  calcified. 

As  a  result  of  the  treat- 
ment of  the  nodules  with  the 
lo  per  cent  cold  solution  of 
caustic  potash,  a  very  profuse 
and  intricately  branched  fun- 
gus became  apparent.  The 
branching  is  of  an  irregular 
order.  In  places  there  is  seen 
in  the  filament  a  central  axis, 
which  takes  the  stain,  and 
around  this  appears  a  trans- 
parent or  hyaline  sheath  of 
varying  size. 

In  certain  of  the  teased 
preparations  ( Biondi-Ehrlich 
stain)  the  wall  of  the  filament, 
instead  of  being  smooth  and 
homogeneous,  appears  rough- 
ened, as  if  covered  with  verj' 
minute  but  numerous  spinous  processes. 

In  the  sections  of  the  tissue  in  which  the  fungus  appeared 
the  substance  of  the  filament  was  not  uniform.  In  places  it 
was  drawn  together  in  an  irregular  manner,  with  intervening 
clear  spaces  of  greater  or  less  area. 


Fig.  52.     The  fungus.      Toluidin 
blue  preparation.     {Fish.) 


Plate  V. 


Fungus. 


MORBID    ANATOMY 


225 


In  some  places  the  filaments  show  distinct  septa,  but  the 
latter  are  not  common.  Some  of  the  club-like  endings, 
especially  those  that  are  elongated,  show  a  septum  at  the 
union  wnth  the  filament  proper.  Scattered  among  and  coiled 
around  the  ordinary  filaments  there  have  been  observed  much 
more  slender  ones  apparently  devoid  of  anj-  external  sheath. 


li 


Fig.  53.  A  section  through  a  nodule  shounng  its  dense  texture,  with 
a  portion  of  its  peripheral  zone  made  tip  of  hyphce  with  leucocytes  inter- 
spersed. Methylene  blue  a7id  eosin  stain.  N^o.  4  ocular,  Smm.  objective. 
Camera  lucid  a .     ( Fish . ) 


226  LEECHES 

There  have  also  been  observed  numerous  small  circular 
bodies  of  inconstant  size.  The}^  have  been  seen  lying  freely 
in  the  meshes  of  the  mycelium  and  also  closely  applied  to  the 
filaments.  These  bodies  are  not  spherical,  but  thin  and  flat- 
tened, and  some  of  them  present  a  curved  appearance,  convex 
on  the  outer  side  and  concave  on  the  inner  side.  They  sug- 
gest the  possibility  of  having  been  closely  applied  to  the  fila- 
ments and  have  something  of  a  scale-like  arrangement.  With 
possibly  one  exception,  no  trace  of  blood  vessels  has  been 
found  in  the  nodules. 

In  the  circumnodular  tissue  pathologic  conditions  exist 
consisting  of  certain  areas  of  tissue  necrosis. 

There  is  an  infiltration  of  the  connective  tissue  with  a 
great  number  of  wandering  cells.  In  some  places  there  are 
well-defined  nests  in  the  stroma  of  the  connective  tissue, 
simulating,  perhaps,  a  cancerous  appearance.  The  character 
of  the  cells,  which  present  a  curiously  vacuolated  condition, 
would,  however,  tend  to  eliminate  this  view.  The  vacuoles 
vary  in  number  and  size,  the  average  number  being  lo  to  12 
in  a  cell. 

In  some  preparations  numerous  leucocj'tes,  of  the  mono- 
nuclear and  poly  nuclear  variety,  had  drifted  away  from  the 
nodule.  They  were  for  the  most  part  elongated,  and  in  all 
the  nucleus  or  nuclei  appeared  to  be  in  a  healthy  condition. 
The  cells  contained  numerous  small  bodies,  which  took  a  deep 
orange  color  with  the  Biondi-Ehrlich  stain.  In  places  adjacent 
to  these  leucocytes  there  were  frequently  noticed  a  number  of 
these  small  bodies  apparently  lying  free  in  the  tissue.  No 
definite  cell  wall  was  distinguishable  in  the  leucocytes. 

The  vacuolated  cells  are  present  in  greater  numbers  than 
the  heavily  laden  leucocytes.  In  the  lormer  nuclei  were 
present  and  presented  various  phases  of  change.  In  some 
there  is  a  single  nucleus,  which  may  be  circular,  crescentic, 
or  in  the  form  of  a  dumb-bell  ;  in  others  there  may  be  two  or 
more  nuclei  which  in  advanced  cases  appear  only  as  remnants. 
In  extreme  cases  no  nuclei  at  all  are  visible.  The  wall  of  the 
wandering  cell  differs  from  that  of  the  leucocytes  proper  in 
possessing  an  appreciable  thickness.     This  thickened  boundary 


MORBID    ANATOMY  227 

apparaiitly  gives  considerable  rigidity  to  the  cells,  as  nearly  all 
of  them  are  approximately  circular  in  form.  Their  average 
diameter  is  about  8  microns.  In  one  specimen  there  appeared  to 
be  large  giant  cells,  measuring  from  12  to  1 8  microns  and  appar- 
ently possessing  quite  a  distinct  cell  wall.  Within  each  giant 
cell  there  is  some  appearance  of  vacuolated  cells,  each  with  a 
single  nucleus  and  fairly  well-defined  cell  boundary.  As  many 
as  eight  or  ten  of  these  nuclei  have  been  counted  in  a  single 
giant  cell.  There  is  the  possibility  that  these  apparent  giant 
cells  are  simply  some  of  the  vacuolated  cells  fused  together, 
but  the  nuclei  are  well  defined  and  take  the  stain  very  intensely, 
which  is  not  commonly  the   case   in   the   ordinary   vacuolated 

cells. 

The  connective-tissue  cells  surrounding  the  nodule  show 
marked  signs  of  degeneration,  their  cytoplasm  in  most  cases 
being  extremely  vacuolated.  Among  these  connective-ti.ssue 
cells,  which  for  the  most  part  are  quite  branching  and  elon- 
gated, is  another  class  of  cells  which  are  in  general  of  an  oval 
or  elliptical  form.  The  noteworthy  appearance  of  these  cells 
is  the  presence  of  numerous  dots  in  the  cytoplasm  which  take 
the  methylene  blue  and  toluidin  blue  stains  very  deeply.  The 
appearance  is,  indeed,  very  much  as  if  the  cells  were  filled 
with  micrococci.  These  are  the  granule  cells  of  Waldeyer,  or 
still  further  differentiated  as  the  plasma  cells,  in  contradis- 
tinction to  the  "mastzellen"  or  "food"  cells,"  which  indicate 
an  exalted  degree  of  nutrition.  The  nucleus  of  the  plasma 
cell  takes  the  stain  very  slightly,  or  not  at  all,  and  is  almost 
entirely  obscured  by  the  numerous  "granules"  in  the  cyto- 
plasm. These  cells  are  well  differentiated  by  the  toluidin  blue 
stain,  as  they  take  a  deep  purple  color,  while  the  surrounding 
cells  are  blue. 

Bitting  has  figured  the  jaw  bone  of  a  horse  quite  exten- 
sively affected  with  this  disease.  He  believes  that  the  lesions 
about  the  mouth  result  from  the  animal  biting  the  affected 
areas  on  the  body. 

Neyrick  reports  finding  the  inflammatory  growths  in  the 
lungs  of  an  affected  subject  and   Burke  has  reported  them  in 


228  PNEUMOMYCOSIS 

the  liver.  There  are  no  other  lesions  described  in  the  internal 
organs  although  Neal  writes  that  any  tissue  may  be  invaded. 
§  175.  Treatment.  On  the  ground  that  the  fungus  sup- 
posed to  be  the  cause  of  this  disease  may  be  closely  related  to 
the  ray  fungus  of  actinomycosis,  the  use  of  iodide  of  potas- 
sium has  been  recommended.  It  is  reported  to  be  fairly  suc- 
cessful. The  efficiency  of  this  drug  as  a  specific  needs  further 
confirmation. 

DESCRIPTION    OF    PLATE    V. 

Fig.   I.     Shozving  a  young  fnyigus  embedded  in  the  tissue  (lip.) 

Fig.   2.     Showi7ig  scale  like  bodies  embracing  the  filaments. 

Fig.  3.  Shozuing  young  branches  of  the  fungus,  and  in  one  place 
the  transparent  sheath.     Hematoxylin  preparation. 

Fig.  4.  Mycelium  zvith  scale-like  bodies  lying  among  the  filaments. 
Hem.atoxylin . 

Fig.  5.      /  'acuolated  filaments.     Hematoxylin. 

Fig.  6.  Branches  shozving  a  zvcll-developed,  transparent  sheath.  In 
places  the  axis  of  the  branch  is  disconnected  and  occasionally  there  is  a 
faint  sign  of  a  septum.     Hematoxylin. 

No.  4  ocular,  2 mm.  objective.     Camera  lucida.    {After  Fish) 

REFERENCES. 

1.  Bitting.  Leeches  or  leeching.  Bulletin  No.  2^,  Florida  Agri- 
cultural  Experiment  Station.     1S94. 

2.  Fish.  A  histological  investigation  of  two  cases  of  an  equine 
mycosis,  with  a  historical  account  of  a  supposed  similar  disease  called 
bursattee  occurring  in  India.  Annual  Report,  Bureau  of  Animal  In- 
dustry, U.  S.  Dept.  of  Agriculture.  1895-6.  p  229.  (This  report  contains 
full  bibliography  to  literature  on  Bursattee.  ) 

3.  Neal.  "Leeching  of  horses  and  cattle.  Annual  Report,  Bureau 
of  Animal  Industry,  U.  S.  Dept  of  Agriculture.     1887-8.     p.  489. 


PNEUMOMYCOSIS. 


§  176.  Species  of  fungi.  The  literature  contains  a  num- 
ber of  reports  of  cases  of  mycosis  in  the  lower  animals  as  well 
as  in  man  due  to  infection  with  different  moulds.  The  genus 
Aspergillus  seems  to  infect  and  to  produce  lesions  in  animals 
more  frequently  than  the  members  of  other  genera.  In  fact, 
Aspergillus  fiimigatus  seems  to  be  the  only  important  pathogenic 
species.     The  lesions  encountered  as  a  result  of  its  invasion  are 


ASPERGILLUS  229 

largely  restricted  to  the  respiratory  tract.  Pneumomycosis 
has  been  reported  in  a  number  of  cases.  Cadeac,  Schneidemiihl, 
Friedberger  and  Frohner,  Ostertag  and  Kilt  have  all  called 
attention  to  mycotic  pneumonia.  Renon  considers  the  lesions 
resulting  from  aspergillus  infection  as  a  pseudo-tuberculosis 
which  he  would  designate  as  "Aspergillar  tuberculosis." 
Aspergillar  pneumonia  is,  however,  quite  rare. 

§  177.  Description  and  method  of  cultivation  of  the 
mould.  The  aspergillus  fungus  is  readily  cultivated  artificially. 
It  grows  on  most  of  the  ordinary  culture  media  used  in  bac- 
teriology if  the  reaction  is  acid  ;  it  develops  poorly  in  alkiline 
media.  The  well-known  Raulin's  fluid  is  reported  to  be  the 
best  medium  for  its  cultivation,  especially  where  the  aspergillus 
must  be  isolated  from  mixed  growths,  as  in  the  examination 
of  sputum.  Sabouraud's*  solution  of  maltose  also  gives  good 
results. 

For  ordinary  use  potato,  with  or  without  glycerin,  gives 
excellent  results.  A  paste  made  by  rubbing  up  crumbs  of 
stale  bread  in  water  is  also  a  good  medium.  Growth  is  said 
to  be  more  rapid,  however,  in  Raulin's  fluid  than  in  any  other 
medium,  the  mycelium  appearing  in  from  five  to  twelve  hours 
and  spores  forming  in  from  twelve  to  fifteen  hours.  The 
o-rowth  is  first  a  velvety  white,  soon  becoming  a  delicate  bluish 
ereen.  which  s,rows  darker.  On  Raulin's  fluid  it  changes 
after  some  days  to  a  dark  brown.  Cultures  on  potato  retain 
the  green  color  for  a  long  time,  while  those  on  bread  paste 
become  brown. 

The  fungus  retains  its  vitality  in  cultures  for  many 
months  unim pared.  Its  development  has  been  reported  when 
inoculated  from  cultures  three  or  four  years  old.  vSpores 
do  not  form  in  a  temperature  below  20°  C.  and  like  the 
mycelium  they  require  free  access    to  oxygen  for  their  best 

*The  formula  recommended  by  Ravenel  is  as  follows,  viz.: 
Maltose,  3.70  grams. 

Peptone,  0.75  grams. 

Distilled  water,        ico.oo  c.  c. 
To  this  may  be  added  gelatin  or  agar  to  solidify  it,  the  latter  being  pre- 
ferable, as  the  aspergillus  grows  best,  and  forms  fruit  best  at  37°  1039°  C. 


230  PNEUMOMYCOSIS 

development.  They  measure  2.5  to  3/7  in  diameter.  In 
nature  the  spores  are  widely  distributed  but  seem  to  be 
especialh-  abundant  in  grain  and  vegetable  matter.  They 
have  considerable  power  of  resistance  to  heat  and  to  chemical 
agents.  They  are  killed  by  a  temperature  of  60°  C.  in  five 
and  one-half  hours.  In  moist  heat  and  in  a  solution  of 
bichloride  of  mercury  i  to  1,000  they  are  destroyed  in  fifteen 
minutes. 

Aspergillus  funiigatus  is  differentiated  from  other  species 
by  its  color  in  cultures,  the  high  temperature  at  which  it 
grows,  the  size  of  its  spores  and  by  its  pathogenesis.  Asper- 
gillus glaucus  is  the  one  most  likely  to  be  confounded  with  it. 
It  may  be  differentiated  from  A.  fiunigafus  by  its  ability  to 
grow  at  low  temperatures,  its  delicate  green  color,  the  large 
diameter  of  its  spores — 9  to  15/^ — and  its  lack  of  pathogenic 
power. 

The  mode  of  infection  is  through  the  respiratory  tract. 
Only  a  small  number  of  the  spores  inspired  are  able  to  reach 
the  alveoli,  the  greater  number  of  them  being  arrested  in 
the  tracheal  and  bronchial  secretions.  Hildebrant  has  shown 
that,  having  reached  the  alveoli,  they  penetrate  the  epithelial 
lining  without  difficulty.  Both  animals  and  man  seem  to 
possess  immunity  to  intestinal  infection.  Renon  has  produced 
it  only  a  few  times  experimentally. 

The  aspergillus  does  not  form  a  toxin.  Its  pathogenic 
power  is  due  entirely  to  lesions  produced  by  the  masses  of 
mycelium  which  cause  a  necrosis  of  the  cells  and  a  leucocytic 
reaction  which  diminishes  the  functions  of  the  organs,  the 
final  result  being  an  enfeebled  condition  of  the  animal  and  a 
lessened  resistance  to  hurtful  influences.  When  fruit  hyphae 
can  form,  the  myriads  of  spores  given  off  by  them  may  be 
carried  to  other  parts  of  the  organ.  In  this  way  the  foci 
rapidly  multiply  and  practically  the  entire  organ  becomes 
invaded.  The  opinion  held  by  some  authors  that  in  the  mould 
mycoses  there  is  "no  fructification  or  actual  multiplication" 
of  the  infecting  agent  and  that  the  "number  of  the  diseased 
foci  corresponds  exactly  with  the  number  of  spores  introduced" 
is  erroneous  both  for  the  disease  naturallv  contracted  as  well  as 


MORBID    ANATOMY  23 1 

for  the  experimental  form.  In  the  produced  lesions,  fruit  forma- 
tion is  exceptional  ;  but  it  has  been  observed  by  Renon  to  take 
place  only  where  there  is  full  communication  with  the  air.  It 
has  been  observed  only  in  the  lung.  It  is  extremely  rare  for 
aspergillosis  to  pass  from  one  animal  to  another.  The  infec- 
tion can  only  take  place  with  the  spores. 

Recently  Pearson  and  Ravenel  have  described  a  very  inter- 
esting case  of  pneumomycosis  in  a  cow  due  to  A.  fiimtgaius. 
As  this  seems  to  be  the  only  carefully  described  case  in  this 
species  of  animals  listed  in  this  country  their  description  of  the 
symptoms  and  lesions  is  very  largely  incorporated  here.  The 
case  was  in  a  Jersey  cow  six  years  old.  She  had  been  in  bad 
condition  for  six  months  prior  to  bringing  her  to  the  Veteri- 
nary Hospital  where  she  was  tested  with  tubercuhn  with 
no  reaction.  At  this  time  she  did  not  eat,  was  weak  and 
depressed,  respiration  labored  and  from  40  to  60  per  minute. 
Pulse  rapid.  Percussion  of  the  chest  walls  gave  a  sound  that 
if  anything  was  clearer  and  louder  than  the  normal  percus- 
sion sound.  Upon  auscultation  it  was  found  that  the  vesicular 
and  bronchial  murmurs  were  considerably  increased  in  inten- 
sity and  accompanied  here  and  there  by  sibilant  rales.  She 
coughed  violently  at  times.  Six  days  after  she  came  to  the 
hospital  the  breathing  became  more  rapid  and  difficult  and  the 
pulse  very  much  accelerated.  The  animal  did  not  eat,  grew 
weak  rapidly  and  died  four  days  later,  or  ten  days  after  admis- 
sion to  the  hospital. 

i^  178.  Morbid  anatomy.  The  anatomical  changes 
given  here  are  restricted  to  the  case  of  Pearson  and  Ravenel. 
The  animal  was  much  emaciated.  The  mucous  membrane  of 
the  small  intestine  was  catarrhal  and  showed  a  small  amount 
of  erosion.  All  the  organs  were  normal  except  the  lungs. 
The  most  striking  features  on  external  examination  was  the 
extreme  amount  of  emphysema.  The  lobules  were  separated 
from  each  other  by  3  to  5  mm.  and  even  at  some  distance  from 
the  borders  one  could  see  through  these  crevices  by  transmitted 
light.  On  the  surface,  the  sub-pleural  connective  tissue  was 
di.stended  by  large  blebs.  Upon  palpation  the  lung  crackled 
and  numerous  hard  nodules  could  be  felt.     On  section  numer- 


232  PNEUMOMYCOSIS 

ous  dark  red  nodules  appeared  in  the  surrounding  normal 
tissue.  In  each  lung  there  were  from  fifty  to  sixty  of  these 
nodules,  from  5  to  12  mm.  in  diameter.  Most  of  them  were 
dark  red  and  closely  resembled  partially  organized  blood  clots. 
However,  on  crushing  a  portion  in  glycerin  between  two 
slides  and  examining  under  the  microscope,  they  were  found 
to  be  made  up  almost  entirely  of  a  felted  network  of  mycelial 
threads.  Between  these  large  nodules  there  were  numberless 
smaller  areas  of  much  the  same  color,  i  to  2  mm.  in  diameter, 
not  perceptible  to  the  touch  as  nodules  but  which  were  of  the 
same  character  and  were  no  doubt  foci  of  recent  origin.  These 
were  seen  especially  well  in  portions  of  the  lung  which  were 
preserved  by  Pick's  method,  the  slight  bleeching  of  the  tissue 
bringing  them  into  relief.  On  opening  some  of  the  inter- 
lobular emphysematous  spaces,  small,  whitish,  mouldy  look- 
ing patches  were  noticed  which  bordered  the  cavity.  Scrapings 
of  these  patches  were  made  up  entirely  of  perfect  fruit  hyphae, 
with  myriads  of  spores.  The  diagnosis  of  a  mould  mycosis 
was  in  this  way  made  at  once  and  confirmed  by  cultures  and 
examination  of  sections.  Cultures  were  made  on  glycerinated 
potato,  bouillon  and  plain  agar,  by  opening  a  nodule  with 
sterile  instruments  and  tearing  out  a  small  portion  of  the 
center,  which  was  transferred  to  the  culture  tubes  and  placed 
in  an  incubator  at  39°  C.  Abundant  growth  was  obtained  on 
the  potato  by  the  end  of  thirty-six  hours,  white  at  first  but 
soon  changing  to  a  yellowish  and  later  to  a  dark  green.  The 
growth  in  the  bouillon  and  agar  was  slow.  Plates  and  flasks 
of  bread  paste  were  made,  and  these  with  potato  were  employed 
for  all  subsequent  cultures.  The  formation  of  the  fruit  hyphae 
was  studied  and  the  spores  measured  a  number  of  times,  being 
from  2.5  to  3.5//  in  diameter.  By  these  means  the  culture 
was  identified  as  the  aspergillus  fumigalus.  The  experiments 
on  other  animals  were  limited  to  the  inoculation  of  one  rabbit, 
into  the  aural  vein  of  which  one-half  cubic  centimeter  of  a 
suspension  of  the  spores  was  injected.  The  animal  died  in 
forty-four  hours  and  from  the  liver  and  kidneys  cultures  were 
recovered.  All  of  the  organs  were  examined  in  sections,  but 
the  mycelium  was  detected  in  two  only. 


HISTOLOGY  233. 

Microscopic  examijiation.  The  nodules  were  hardened  and 
embedded  some  in  collodion  and  some  in  paraffin.  Various 
staining  methods  were  tried,  hematoxylin  and  eosin,  carbol- 
thionine,  Gram  and  lithium  carmine  with  Weigerts  fibrin 
stain.  Good  results  were  obtained  with  all,  but  the  carmine 
and  Weigert  gave  the  most  beautiful  picture  and  by  this 
method  the  fungus  was  most  perfectly  demonstrated,  the  spores 
and  mycelium  taking  on  a  deep  purple  color.  The  histology 
was  studied  largely  in  sections  stained  with  hematoxylin  and 
eosin.  The  bronchial  epithelium  was  normal  in  places,  but, 
for  the  most  part,  the  columnar  cells  have  been  replaced  by  a 
sort  of  membrane,  which  appears  to  be  made  up  almost  entirely 
of  a  felt-work  of  mycelial,  threads.  From  this  membrane 
hyphge  grow  out  into  the  lumen  of  the  bronchus,  and  here, 
owing  no  doubt  to  the  supply  of  air,  fruit  hyphae  arise,  with 
perfect  sterigmata  and  spores.  There  is  no  cellular  nor  other 
exudate  and  very  little  debris.  The  under  surface  of  this 
membrane  is  of  looser  texture,  and  contains  some  cellular  in- 
filtration made  up  of  round  cells,  leucocytes,  proliferated  con- 
nective tissue  cells  and  red  blood  corpuscles.  The  adjacent 
structures  are  closely  filled  with  a  cellular  infiltration  with  a 
quantity  of  mycelium  of  the  same  description,  this  extending 
to  the  neighboring  alveoli  which  under  low  power  appear  to 
have  preserved  their  outline  but  with  greater  amplification  are 
seen  to  have  lost  all  their  normal  structure,  showing  clumps 
of  homogeneous,  irregular  masses  which  stain  faintly  with 
eosin  and  are  probably  of  connective  tissue  origin. 

In  these  areas  the  mycelium  followed  the  alveolar  wall  as 
a  trellis,  the  tissue  seeming  to  afford  no  obstacle  to  its  advance. 
Within  the  alveoli  is  a  finely  granular  debris,  with  some 
coarser  particles,  probably  the  remains  of  cells.  In  sections 
stained  with  carbol-thionine  large  numbers  of  mast  cells  are 
seen  in  the  alveolar  walls.  Bordering  these  degenerated  areas 
are  alveoli  which  have  retained  their  normal  structure  and  are 
filled  with  a  network  of  fibrin  holding  in  its  meshes  a  few 
cells.  In  other  parts  of  the  sections  are  areas  resembling  those 
just  described,  but  in  which  all  anatomical  land  marks  have 
been  destroyed,  so  that  it  is  impossible  to  tell  whether  or  not 
the  spaces  seen  are  bronchi. 


234  PNEUMOMYCOSIS 

Some  sections  show  a  widespread  interstitial  and  alveolar 
hemorrhage,  the  blood  showing  a  considerable  increase  in  the 
number  of  leucocytes.  The  capillaries  are  congested  and  areas 
of  oedema  with  thickening  of  the  alveolar  walls  are  not  un- 
common. 

There  is  peribronchitis  and  arthritis,  while  in  some  sec- 
tions arterial  thrombosis  is  seen,  the  thrombus  being  penetrated 
by  mycelium,  though  no  fruit  is  found.  Areas  are  also  found  in 
which  the  alveoli  are  filled  with  a  cellular  exudate  producing 
consolidation  and  thickening  of  the  alveolar  walls. 

Emphysema,  both  interstitial  and  vesicular,  is  marked 
and  often  extreme.  Around  the  borders  of  the  interstitial 
cavities  is  a  distinct  zone  made  up  of  red  blood  cells,  leucocytes 
and  hemogeneous  material,  which  is  yellowish  both  in  fresh  as 
well  as  in  stained  sections.  These  areas  contain  very  little 
mycelium.  All  sections  show  a  small  amount  of  anthracosis. 
The  appearance  of  sections  varies  in  different  nodules  as  they 
are  taken  further  and  further  away  from  the  center.  In 
general  the  fungus  is  thickest  at  the  center,  so  thick  in  many 
instances  that  the  lung  tissue  is  hidden  entirely  and  grows 
less  as  we  go  outwards.  The  tissue  changes  noted,  take  place 
in  a  zone  beyond  the  greatest  growth  of  the  fungus.  In  other 
nodules  the  fungus  is  evenly  distributed  throughout  following 
the  alveolar  walls.  In  these  the  tissue  changes  are  slight. 
At  times  the  fungus  grows  in  dense,  brush  like  clusters, 
closely  resembling  actinomycosis  under  low  amplification. 
This  form  is  considered  to  show  a  marked  reaction  and  resist- 
ance on  the  part  of  the  animal  and  a  lowered  vitality  in  the 
fungus.  When  found  it  indicates  that  the  aspergillosis  is  a 
primary  and  not  a  secondary  or  terminal  affection.  No  giant 
cells  were  found  in  any  section. 

Fruit  formation  was  not  observed  in  the  substance  of  the 
tissues  at  any  time.  It  was  observed  most  frequently  in 
bronchi,  which  were  for  the  most  part  denuded  of  their  epi- 
thelium and  next  in  emphysematous  cavities,  where  it  could 
be  detected  in  clusters  by  the  naked  eye.  Fruit  was  found 
in  sections,  in  .spaces  the  nature  of  which  it  was  impossible  to 
determine  accurately.     Wherever   the   formation  of  fruit  was 


Plate  VI. 


Composite  drawing  of  section  of  Lung  through    nodule    of    aspergillus    origin.     F.    fibrin 
in  alveoli.     S.  fruit  hyphae  and  spores  of  fungus.     (Ravenel.) 


HISTOLOGY  235 

seen,  there  were  innumerable  free  spores  as  well  as  those  still 
attached  to  the  sterigmata,  but  in  no  case  were  spores  detected 
in  the  substance  of  the  tissues. 

In  many  sections,  especially  those  from  near  the  center 
of  the  nodules,  the  mass  of  mycelium  was  so  dense  that 
the  structure  of  the  tissues  was  obscured.  Besides  the  dense 
growths  resembling  actinomycosis  already  described,  other 
brush  like  clusters  not  unlike  them  were  frequently  seen. 
These  differ  from  the  former  in  being  somewhat  less  com- 
pact, and  that  from  their  periphery  numerous  hyphae  run  out 
into  the  surrounding  tissues,  whereas  in  the  actinomycotic 
form  the  masses  are  sharply  defined  and  only  here  and  there 
a  few  threads  grow  out  beyond  the  cluster.  Their  appearance 
suggests  that  the}^  may  be  actinomycotic  forms  which  have 
finally  overcome  the  resistance  of  the  tissues.  Emphysema  is 
less  marked  in  the  neighborhood  of  the  latter. 

The  cow  was  examined  carefully  for  the  lesions  of  tuber- 
culosis and  in  one  lung  some  four  or  five  caseous  and  calcareous 
nodules  i  cm.  in  diameter  were  found  in  which  tubercle  bac- 
teria were  demonstrated,  but  no  mycelium  could  be  detected. 
In  no  part  of  the  lung  was  there  coexistence  of  the  two 
infections. 

The    fact    that    the  animal   did  not   react  to    tuberculin, 

though  tuberculosis  was   present,  is   noteworthy  and  suggests 

that  the  mould  infection  may  interfere  with  the  test.      It  adds 

a  possible  source  of  error  in  the  tuberculin  test  to  be  guarded 

against. 

REFERENCES. 

1.  Arwine  AND  Lamb.  A  fifth  case  of  "fungous  foot"  in  America. 
The  Am  Journ .  of  Med.  Sciences.     Oct.,  1S99. 

2.  DiNWiDDiE.  On  the  toxic  properties  of  moulds.  Bulletin  No. 
10,  Arkansas  Agric.  Exp.  St  a.     May,  1896. 

3.  Flexner.  Pseudo-tuberculosis  Hominis  Streptothricha.  The 
Journal  of  Experimental  Medicine.     Vol.  III.   (1S98)  (Bibliography). 

4.  Ophuls  and  Moffitt.  a  new  pathogenic  mould.  The  Philadel- 
phia Med.  Journal.     June  30,  1900. 

5.  Pearson  and  Ravenel.  A  case  of  pneumonomycosis  due  to 
the  Aspergillus  fumigatus.  The  University  Medical  JMagazine.  Aug., 
1900.      The.  Vet.  Journal,  New  Series.     Vol.11.     (1900)  p.  229. 

6.  Renon.  L'Etude  sur  TaspergiMose  chez  les  animaux  et  chez 
rhomme.     1897. 

7.  Weis.  Four  pathogenic  Touruke  (Blastomycetes).  The  Jour, 
of  Med.  Research.     Vol.  VII.     (1902)  p.  280. 


CHAPTER    VI. 


DISEASES  CAUSED  BY  PROTOZOA. 


TEXAS  OR  SOUTHERN    CATTLE  FEVER. 

Synonyms.  "Red  water' ' ;  Mexican  fever  ;  Spanish  fever  ; 
Splenic  fever,  "  Bloody  Murrain". 

§  179.  Characterization.  Texas  fever  is  an  infectious 
blood  disease  of  cattle,  characterized  by  rise  of  temperature, 
hemoglobinuria,  destruction  of  the  red  blood  corpuscles  and 
the  presence  in  the  blood  of  a  protozoan  parasite  which  is  trans- 
mitted from  animal  to  animal  by  means  of  the  cattle  tick. 

It  is  believed  to  be  identical  with  the  hemoglobinuria  in 
Roumania,  Tick  fever  in  Australia,  and  "La  Tristeza  "  in 
South  America.  It  has  been  named  malaria  des  bovides  by 
Celli  and  Sentori  and  Malaria  Bovine  by  Lignieres.  Although 
it  differs  in  many  ways  from  human  malaria,  the  analogy  is  so 
close  respecting  the  specific  cause,  wide  distribution  and 
means  of  transmission  that  bovine  malaria  seems  to  be  a  very 
suitable  name  for  this  affection.  At  least  it  has  the  advantage 
of  not  stigmatizing  any  locality. 

The  peculiar  and  interesting  feature  of  this  affection  is  the 
fact  that  cattle  raised  in  the  infested  districts  become  im- 
munized so  that  they  do  not  suffer  from  the  disease  but  the}- 
carry  its  specific  organism  in  their  blood.  When  imported 
into  non-infested  districts,  they  transmit  the  virus,  by  means 
of  the  cattle  tick,  to  susceptible  animals,  but  remain  them- 
selves perfectly  well. 

§  180.  History.  There  is  little  knowledge  concerning 
the  early  history  of  this  disease.  With  the  development  of 
commerce,  however,  the  shipping  and  interchange  of  animals 
gradually  came  into  prominence  and  with  it  all,  this  disease 


HISTORY  237 

which  had  long  been   known   in  certain   localities  was   more 
widely  scattered  and  finalh-  it  came  to  be  an  important  barrier 
to  the  cattle  traffic.      In  186S,  the  disease  seems  to  have  made 
its  first  important  impression   upon  the  American  people.      In 
June  of  that  year,  Texas  cattle  were  shipped  up  the  Mississippi 
river  to  Cairo  and  thence  by  rail  into  the  states  of  Illinois  and 
Indiana  where  they  caused  during  the  summer  enormous  losses 
from  this  disease.    Cattle  from  these  states  shipped  east  brought 
the  disea.se  with  them.      The  cattle  commissioners  of  New  York 
and  the  Board  of  Health  of  New  York  City  endeavored  to  check 
the  importation  of  such  cattle.    The  disease  was  carefully  inves- 
tigated at  that  time  but  nothing  beyond  a  very  accurate  descrip- 
tion of  the  gross  lesions  was  obtained.     Later  Dr.  D.  E.  Salmon 
determined  the  boundary  line  between  the   non-infected   and 
the  permanently  infected  districts,  or  what  is  now  known  as 
the  Texas  Fever  line  (vSee  Plate  VII).      In   1889,  the  Bureau 
of  Animal  Industrj-  undertook  a  systematic  investigation  into 
the    nature    of    this    disease,    which    resulted    in    the    same 
year  in  the  discover}-  of  its   specific  cause  by    Dr.  Theobald 
Smith  and  later  the  demonstration  of  the  fact  that  the  disease 
is  transmitted  from  southern  to  northern  cattle  through  the 
medium  of  the  cattle  tick.      Prior  to  this  (1888)  V.  Babes  had 
found  an  intraglobular  parasite  in  the  blood  of  cattle  suffering 
from     an    epizootic    disease    (hemoglobinuria)    in    Roumania. 
\Miile  at  first  these  diseases  were  thought  to  be  different  in 
their  etiology-  the}-  are  now  believed  to  be  identical.      Recently 
a  number  of  investigations  have  been  made  b}-  the  Bureau  of 
Animal   Industry,    the  State   Experiment  Station    and   State 
Board  of  Agriculture  of  Missouri,  the  Louisiana  Experiment 
Station  and  b}-  the  Queensland  Government,  Australia,  for  the 
purpose  of  obtaining  a  practical  method  for  the  production  of 
immunity  against  Texas  fever  in  susceptible  cattle.     Although 
the  results  thus  far  obtained   are  promising  aa  they  are  often 
successful,     the    methods    must    still   be    considered   in    the 
experimental  stage. 

§  181.  Geographical  distribution.  In  the  United 
States  the  distribution  of  Texas  fever  corresponds  with  that 
of  the  cattle  tick  {Bobphilus  bovis).  This  includes,  with  possi- 


238  TEXAS    FEVER 

bly  a  few  small  exceptional  areas,  that  portion  of  the  country 
south  of  the  "Texas  fever  line"  which  is  shown  by  a  red  line 
on  the  accompanying  map  but  which  is  changing  constantly  by 
virtue  of  the  spread  or  elimination  of  the  tick.  It  has  been 
identified  with  the  tick  fever  of  Australia  which  has  become  a 
source  of  great  loss  to  the  cattle  industry  of  that  country. 
Lignieres  has  identified  the  disease  in  South  America  (  Argen- 
tine Republic).  It  is  also  reported  to  be  identical  with  a 
malady  affecting  cattle  along  the  Danube  River,  in  the  Balkan 
provinces  and  in  Southern  Africa.  It  is  restricted,  however, 
to  those  countries  where  the  climate  is  not  sufficiently  severe 
to  destroy  the  cattle  tick  during  the  winter  season  and  where 
the  animals  are  constantly  infested.  Cattle  (genus  Bos)  are 
the  only  animals  which  suffer  from  it. 

§  182.  Etiology.  Texas  fever  is  caused  by  a  microor- 
ganism belonging  to  the  protozoa  and  named  by  Smith,  the 
discoverer,  Pyrosovia  bigeminum.'^  It  is  generally  recognized 
that  Piroplasma 
is  the  proper 
generic  term  and 
it  is  used  by 
writers     on     the  ^^^'  54-     Piroplasma   bigeminiim  in  red  blood 

corpuscles. 
protozoa. 

If  Texas  fever  in  America,  and  hemoglobinuria  in 
Roumania  are  identical,  Babes  was  the  first  to  call  attention  to 
the  existence  of  this  intra-globular  parasite.  It  seems  that 
Dr.  Stiles  in  1867  observed  this  organism  but  failed  to  recog- 
nize its  significance.  It  is  found  in  the  blood  in  cases  of 
Texas  fever  and  it  also  exists  in  the  blood  of  immune  animals 
in  the  tick  infested  districts.  The  life  history  of  this  parasite 
is  not  determined.  In  the  blood  of  the  diseased  animal  they 
appear  in  the  unstained,  fresh  preparation  as  minute  or  larger 
bright  bodies  which  may  be  from  0.5  to  4.0/Y  in  diameter 
according  to  the  form  of  the  disease.     In  the  acute  types  of  the 


*The  genus  of  this  parasite  has  been  changed  to  Piroplasma  by  Pat- 
ton  and  Apiosoma  by  Wandelleck,  to  Auuebosporidies  by  Bonome,  and 
Proteus  virulentissimus  by  Perroncito.  Starcovici  has  named  the  organ- 
ism described  by  Babes   as   Hematococcus,  Babesia  bigeminum  bovis. 


ETIOLOGY 


239 


Fig.  55.  Coccus 
form  of  Piroplasma 
bigemintim. 


disease  certain  of  the  red  corpuscles  contain  pale  or  brighter 

pyriform  shaped  bodies.  One  end  of  each 
body  is  broad  and  rounded,  the  other  taper- 
ing and  pointed.  Usualh-  there  are  two  of 
these  bodies,  both  of  the  same  size  in  a  cor- 
puscle. More  rarely  there  is  but  one, 
although  four  are  occasionally  observed 
(Fig.  57).  When  two  are  present  the 
tapering  ends  approach  each  other  and 
usually  they  are  joined  while  the  other 
ends  may  point  in  any  direction.  Several 
forms  have  been  noted  varying  from  a 
round  to  a  pyramidal  outline.  The  small  and  often  the  larger 
bodies  have  been  ob.served  to  change  their  position  within  the 
red  corpuscle.  Smith  has  noted  that  the  amoeboid  bodies 
observed  w^ere  apparently  single  within  the  corpuscle.  In 
dried  and  heated  cover-glass  preparations  stained  with  alka- 
line methylene  blue,  these  parasites  are  colored  distinctly.  They 
are  also  stained  with  carbol  fuchsin  and  with  hemotoxylin. 
As  a  rule  they  stain  more  deeply  in  pre- 
parations made  for  internal  organs  than 
they  do  in  those  from  the  living  blood. 
In  the  capillaries  of  the  congested 
organs,  the  blood  corpuscles  contain 
many  more  parasites.  Smith  has  noted 
in  one  case  from  2  to  3  per  cent  of  in- 
fected corpuscles  in  the  circulating  blood 
but  in  cover-glass  preparations   made  at 

the  autops}'  quite  different  results,  viz. : 

, ,  11-1  1  ui       1       f    n.  Fig.  56.    Blood  from 

in    the    skeletal    muscles,    blood    01    the    ...  , 

kidney   showing   para- 

right  heart,  and  blood  from  the  bone  mar-  ^^^^^  ^j-  xexas  fever. 
row  (.sixth  rib)  very  few  infected  corpus-  {Smith). 
cles  ;  in  the  blood  from  the  left  heart  and  lung  tissue  from  2 
to  3  per  cent  of  infected  corpuscles  ;  in  the  spleen  5  per  cent  ; 
in  the  liver  and  kidney  tissue  from  10  to  20  per  cent ;  and  the 
hyperemic  fringes  of  the  omentum  and  the  heart  muscle  50 
per  cent  of  the  corpuscles  were  infected.     In  other  cases  the 


240 


TEXAS    FEVER 


Fig.  57.    Cover-glass  pre- 


blood  corpuscles  in  the  capillaries  were 
more  and  in  still  others  less  exten- 
sively infected.  In  the  living  blood 
the  parasites  were  p^-riform,  but  in 
the  post  mortem  specimens,  they  were 
more  nearly  round.  In  the  mild  type 
of  the  disease  from  5  to  50  per  cent  of 
the  red  corpuscles  in  the  circulation 
are  infected  for  a  period  of  from  one 
to  five  weeks.  The  parasite  is  round 
(coccus  form).  In  the  fresh  prepa- 
rations it  is  seldom  seen  ;  rarely  it  can 
be  detected  as  a  pale  spot  about  o.5yU 
paratio7i  from  kidney.  Cor-  in  diameter  at  the  periphery  of  the 
puscles  shoiving  piroplas-  corpuscle.  In  stained  (alkaline  me- 
ma,  coccus  form.  (-^-^^/M)  •  t|^y]ene  blue)  preparations,  the  para- 
sites appear  as  round  coccus-like  bodies  from  0.2  to  0.5//  in 
diameter.  They  are  situated  within  the  corpuscle  on  its 
border.  As  a  rule  only  one  is  found  in  a  corpuscle.  Some- 
times a  division  was  evident  separating  the  para- 
site into  two  parts.  They  must  be  differentiated 
from  somewhat  similarly  looking  bright  bodies 
which  are  seen  in  the  corpuscles  of  healthy 
blood  during  different  seasons  of  the  year. 

Concerning  the  life  history  of  this  parasite, 
Smith  considered  the  intraglobular  stage 
hypothetically  the  swarming  stage,  which  pre- 
cedes the  peripheral  coccus-like  bodies  and  the 
pyriform  and  spindle  shaped  bodies  w^hich  de- 
velop from  the  divided  coccus-like  peripheral 
forms.  The  free  bodies  are  the  parasites  set 
free  after  they  have  reached  the  preceding 
stage  bj'  disintegration  of  the  infected  corpus- 
cles. They  are  most  commonly  found  in  the  kidney.  The 
reproductive  stage  has  not  been  recognized. 

§  182.  Infection.  Although  practical  stockmen  had  long 
looked  upon  the  tick  as  the  source  of  infection  it  remained  for 
Smith  and  Kilborne  to  experimentally  demonstrate  that  so  far 


Fig.  58. 
Blood  in  cap- 
illaryof  heart 
showing  Pi- 
rop  la  s  in  a. 
(Smith). 


INFECTION 


241 


as  known  the  cattle   tick  {Bodphilus  bovis)-'^  is  the  sole  carrier 
of  the  parasite.    It  was  pointed  out  by  them  that  when  southern 

cattle  were   freed   from    ticks 


ss?^ 


thev 


together 


Fig.  59.  Sexually  mature  male 
tick  after  the  last  moult,  dorsal 
viezv.     {Sm-ith.) 


would  not  when  kept 
in  small  enclosures 
transfer  the  disease  to  sus- 
ceptible animals,  but  that 
when  susceptible  cattle  became 
infested  with  the  ticks  either 
b}'  grazing  in  infested  pastures 
or  by  having  placed  upon  them 
young  ticks  hatched  in  the  lab- 
oratory the  disease  appeared.! 
The  infection  of  Northern  cattle  with  Texas  fever  by 
Southern  animals  consists  therefore  in  first  infesting  them  with 
the  cattle  tick.  The  number  of  ticks  necessary'  to  carr}'  the 
disease  is  small  so  that  frequently  they  will  not  be  observed 
unless  the  sick  animals  are  carefully  examined.  The  life 
cycle  of  the  tick  will,  therefore,  explain  the  variation  in  the 
time  elapsing  between  the  exposure  of  northern  to  .southern 
cattle  and  the  appearance  of  the  disease.  Starting  with  tick 
infested  animals  placed  with  native  cattle  in  a  northern  pasture 
the  adult  female  ticks  drop  to  the  ground  almost  daily  so  that 
the  following  life  cycle  maj'  be  assumed  to  begin  at  once. 


*This  tick  was  first  described  by  C.  V.  Riley  in  1S6S  as  Ixodes  bovis. 
Later,  Cooper  Curtice  investigated  this  parasite  (Bioiogy  of  the  Cattle 
Tick,  Journ.  Comp.  Med.  and  Veterinary  Archives,  July,  1891,  Jan.,  1892) 
and  gave  it  the  generic  name  of  Boop/it  I  us  (ox  loving).  This  seems  to 
be  the  only  species  of  cattle  tick  which  transmits  the  parasite  of  Texas 
fever. 

•fit  is  interesting  to  add  the  results  of  an  experiment  conducted  by 
Dr.  Cooper  Curtice  in  the  Bureau  of  Animal  Industry  which  shows  the 
neviessity  of  the  tick  in  inoculating  cattle.  In  a  tick  infested  district  in 
the  South,  a  field  was  cleared  of  ticks  by  fencing  and  keeping  cattle  off 
for  a  year.  Susceptible  northern  cattle  were  transported  to  and  placed 
in  this  field  where  they  thrived  for  a  season.  The  second  year  they  were 
placed  in  a  second  cleared  pasture  where  they  kept  well  for  another 
year.  The  third  year  they  were  placed  in  a  tick  infested  pasture  where 
they  died  promptly  of  Texas  fever. 


242 


TEXAS    FEVER 


^-^ 


Fig.  6o.     Pliotograph  of  atiiinal   sick    zvith    Texas  fever. 
graphed  bv  Connaway). 


[Photo- 


1.  Adult  ticks  drop   to   the  ground   in  from    i  to  3  days 
after  the  infested  cattle  are  placed  in  the  field. 

2.  Adult  ticks  lay  their  eggs  in  about  7  days  after  drop- 
ping to  the  ground. 

3.  Eggs  are  hatched  in  about  20  days  after  they  are  laid. 

4.  Young  ticks  crawl  upon  cattle  from  i  to  several  days 
after  the}^  are  hatched. 

5.  In  about  10  days  from  the  time  the  young  ticks  crawl 
upon  the  susceptible  cattle  the  rise  of  temperature  appears. 

The  length  of  time  that  must  elapse  (period  of  incubation) 
from  the  exposure  of  susceptible  cattle  to  the  development  of 
the  disease  depends  on  whether  or  not  the  whole  life  cycle  of 
the  tick  must  be  passed  or  part  of  it  has  alread}'  gone  by. 
If  susceptible  animals  are  placed  in  a  pasture  where  the  young 
ticks  are  just  ready  to  crawl  upon  them  the  infection  of  the 
cattle  is  accomplished  at  once  and  the  high  fever  appears  in 
about  ten  days,  practically  the  minimum  time.  It  has  been 
experimentally  demonstrated  that  the  young  ticks  are  able  to 


INFECTION 


H3 


travel  for  a  consider- 
able distance  in  a 
pasture.  In  pasnres 
where  tick  infested 
cattle  are  grazing, 
young  ticks  are  very 
liable  to  be  on  the 
ground  continuously. 
In  est  i  m  a  t  i  n  g  the 
time  to  elapse  after 
the    exposure    to    the  Fig.  6i.     Sexually  viature  female  after 

tick    infested    field       H^t"  l^^st  inoiUt,  dorsal  view.     {Si)iilh. ) 
before   the  disease   will   appear,    it    is  necessary,  therefore,  to 
determine  the  exact  stage  in  the  life  circle  of  the  ticks  at  the 
time  when  the  animals  come  in  contact  with  them. 

Small  quantities  of  the  blood  from  immunized  cattle  in  the 
tick  infested  district,  when  injected  into  susceptible  animals 
either  intravenously  or  beneath  the  skin,  will  produce  the 
disease.  While  this  mode  of  infection  rarely  if  ever  occurs  in 
the  natural  order  of  events,  it  may  happen  that  in  case  of  cer- 
tain operations  bits  of  blood  may  be  carried  directly  from  a 
southern  to  a  northern  animal  thus  inoculating  the  latter  with 
the  disease. 

In  the  fall  of 
1898  two  cases  oc- 
curred in  the  prac- 
tice of  Dr.  Ambler 
of  Chatham,  N.  Y. 
The  owner  had  his 
animals  dehorned 
Fig  62.  Eggs  and  young  tick,  just  hatched,  in  December  and 
{Smith.)  soon  afterward  two 

fatal  cases  of  Texas  fever  developed.  The  Piroplasvia  and  the 
characteristic  lesions  were  present.  Inquiry  revealed  the  inter- 
esting fact  that  the  two  animals  which  sickened  and  died  were 
dehorned  immediately  after  two  imported  Southern  cattle.  The 
owner  was  not  aware  of  the  fact  at  the  time  that  these  were 


§ 


& 


244  TEXAS   FEVER 

Southern  bred  cattle,  as  he  had  bought  them  of  a  dealer  in 
Vermont.  More  recently  another  case  of  this  disease  pro- 
duced in  the  same  way  has  been  reported. 

§  183.     Symptoms.     In  the   acute  type  of    the    disease 
which  occurs  during  the  hot  summer  months,  the  onset  is  sud- 
den and  usually   all  animals  exposed  to  the  same  infection 
together  come  down  at  the  same  time.     The  first  indication  of 
the  disease  is  a  rise  of  temperature,  at  first  higher  in  the  after- 
noon than  morning,  but  this  oscillation  is  minimised  later  in 
the  course  of  the  disease  when  the  temperature  remains  high. 
The  temperature  rarely  rises  above   107°  F.     With  a  clinical 
thermometer  the  temperature  can  be   detected    two    or   more 
days  before  there  are  other  symptoms.      The  respiration  may 
rise  to  between  60  and  100  and  the  pulse  may  range  between 
80  and   no  per  minute.       Late  in  the  disease  there  may  be 
hemoglobinuria.     Smith   and  Kilborne  found  it  in  33  out   of 
46  fatal  cases  in  which  urine  was  found  in  the  bladder.     The 
passing  of  the  colored  urine  before  death  was  noted  in  but  four 
of  their  cases.     In  one  of  these  which  showed  hemoglobinuria 
four  days  before  death,  the  urine  in  the  bladder  was  clear  at 
post  mortem.      As  this  condition  seems  to  depend  upon  the 
rapidity  of  the  destruction  of  the  red  blood  corpuscles,  a   slow 
disintegration  may  enable  other  organs  to  dispose  of  the  color- 
ing matter  which  in  a  rapid  destruction  of  the  blood    much  of 
it  may  be  thrown  into  the  urine.     The  urine  contains  small 
quantities  of  albumin.    At  first  the  specific  gravity  may  be  high 
but  later  it  ranges  from   loio  to   1020  and  fails  to  effervesce 
with  acids.      The   color  varies  according  to  the   quantity   of 
hemoglobin.     As  a  rule   there  is  marked  constipation  during 
the  high  fever.     There  is  loss  of  appetite  and  usually  cessation 
of  rumination  with  the  high  fever.     The  blood  is  thin  and 
pale.       The  high  temperature,  hemoglobinuria    and   thinness 
of  the  blood  are  quite  diagnostic  symptoms  of  the  acute    type. 

The  course  of  the  disease  may  vary,  but  the  continuous 
high  temperature  does  not  usually  last  for  more  than  ten  days. 
Death  often  intervenes  in  from  five  to  eight  days.  In  the 
mild,  nonfatal  or  chronic  type  which  was  first  pointed  out  by 
Smith  and  Kilborne  and  which  occurs  in  the  late  summer  or 


MORBID    ANATOMY  245 

autumn,  the  general  symptoms  are  similar  to  those  of  the  acute 
type  except  they  are  not  so  severe  and  are  prolonged  for  a 
greater  length  of  time.  The  parasite  is  of  the  spherical  or 
coccus  form.  The  general  symptoms  are  not  manifested 
unless  the  temperature  goes  above  103°  F.  Hemoglobinuria 
is  not  observed  in  this  type.  Cattle  which  have  passed 
through  an  acute  type  owing  to  the  heated  season  may  have  a 
relapse  in  the  form  of  a  mild  type  in  the  fall.  The  essential 
difference  between  the  two  types  is  found  in  the  different 
stages  of  the  parasite  circulating  in  the  blood.  Unless  the 
temperature  is  taken  and  the  blood  carefully  examined,  mild 
types  of  Texas  fever  would  be  either  overlooked  or  mistaken 
for  any  one  of  a  variety  of  disorders  common  among  cattle. 

^  184.  Morbid  anatomy.  Cattle  which  die  of  Texas 
fever  undergo  post-mortem  changes  very  rapidly.  For  this  rea- 
son the  description  of  lesions  made  some  hours  after  death  may 
be  misleading. 

Externally  the  animal  presents  nothing  abnormal  or  char- 
acteristic of  the  disease.  Rarely  dried  bits  of  blood  may  be 
found  and  also  some  small  slightly  elevated  areas  of  a  bluish 
color.  The  skin  between  the  thighs,  upon  and  about  the  udder 
and  possibly  elsewhere  may  have  cattle  ticks  attached.  It  is  im- 
portant under  ordinary  circumstances  to  look  for  this  parasit£. 
The  subcutaneous  tissue  may  be  more  or  less  yellow  in  color. 
Oedema  of  the  subcutis  over  the  ventral  portion  of  the  body 
has  been  observed.  The  muscles  are  usually  normal  in  appear- 
ance although  frequently  they  are  pale. 

Very  slight  if  any  lesions  have  been  recorded  as  occurring 
in  the  central  nervous  system  and  lungs.  Blood  extravasa- 
tions usually  occur  beneath  the  skin  and  endocardium  espe- 
cially of  the  left  ventricles.  On  the  external  surface  the 
petechiae  occur  for  the  greater  part  along  the  intraventricular 
groove  near  the  base.  The  capillaries  of  the  heart  muscle  are 
packed  with  corpuscles.  Parenchymatous  and  fatty  degenera- 
tion of  the  muscular  fibers  sometimes  exist.  The  right  ven- 
tricle is  distended  with  blood  either  fluid  or  clotted  and  the 
left  one  firmlv  contracted. 


246  TEXAS    FEVER 

In  the  abdominal  cavit}'  there  are  frequentlj^  oedematous 
areas  about  the  kidneys  and  in  the  portal  regions  between  the 
duodenum  and  liver.  The  omentum  is  often  sprinkled  with 
peculiar  hj'peremic  patches  consisting  of  delicate  shreds  of 
vascular  tissue.  This  condition,  however,  is  not  characteristic 
of  Texas  fever. 

Usually  the  most  conspicuous  changes  are  in  the  spleen. 
This  organ  is  much  enlarged  and  increased  from  two  to  four 
times  its  normal  weight.  The  normal  markings,  Malpighian 
bodies  and  trabeculae,  are  hidden  in  the  dark  browish-red, 
glistening  pulp  which  distends  the  capsule.  The  pulp  may  be 
firm  or  it  may  be  in  a  semi-fluid  condition  so  that  it  oozes  out 
if  the  surface  is  cut.  The  enlargement  and  color  of  the  spleen 
are  due  to  an  engorgement  of  red  blood  cells.  There  may 
also  be  present  a  greater  or  less  number  of  large  cells  contain- 
ing granules,  red  corpuscles  or  clumps  of  yellowish  pigment. 
Free  pigment  is  much  more  abundant  than  it  is  in  liealthy 
spleens. 

The  liver  is  extensively  affected.  It  is  enlarged,  con- 
gested, edges  rounded,  the  bile  ducts  more  or  less  distended 
and  the  parenchyma  is  usually  in  a  state  of  fatty  degenera- 
tion. The  color  is  paler  than  normal  and  usually  the  surface 
is  somewhat  mottled.  On  section  the  color  of  the  cut  surface 
is  brownish-yellow  or  it  ma}^  be  mottled  like  the  surface.  The 
mottling  is  due  to  a  discoloration  due  to  degeneration  of  a  zone 
bordering  the  intralobular  vein.  This  zone  varies  in  width 
and  its  peculiar  color  seems  to  be  due  to  a  tendency  to  necrosis. 
It  is  characterized  by  parenchymatous  degeneration  and  the 
loss  of  the  nucleus.  It  may  involve  a  third  or  more  of  the 
lobule.  This  portion  stains  very  feebly  or  not  at  all.  The 
■explanation  for  the  necrosis  of  the  liver  cells  is  suggested  by 
Smith  as  being  due  to  the  plugging  up  of  the  ultimate  bile 
canals  with  solid  bile  which  may  interfere  in  some  way  with 
the  nutrition  of  the  adjacent  liver  cells.  The  bile  stasis  he 
considers  as  a  result  of  the  breaking  up  in  the  capillaries  ot 
the  liver  of  enormous  numbers  of  infected  corpuscles.  This 
results  in  an  abnormal  fluid  containing  an  excess  of  solids 
which    the    bile    ducts    are    unable    to    carry    away.      When 


MORBID    ANATOMY  247 

examined  in  fresh  condition  or  in  sections  of  tissue  fixed  in 
Miiller's  fluid  the  engorgement  of  the  bile  canaliculi  is  seen. 
The  bile  stasis  may  occur  over  a  portion  or  a  whole  of  the 
lobule.  The  gall  bladder  contains  usually  an  abnormal 
quantity  of  changed  bile.  It  is  thick  and  often  semi-solid  in 
consistence  holding  in  suspension  man}-  fiocculi.  It  imparts  a 
deep  yellowish  tinge  to  all  articles  coming  in  contact  with  it. 
Owing  to  the  mucus  which  is  present  it  is  quite  viscid. 

The  changes  in  the  kidneys  vary.  If  death  occurs  early 
the}^  are  usually  enlarged  and  uniformly  darker  than  normal 
throughout.  The  capillaries  are  distended  with  red  corpuscles. 
Parenchymatous  and  fatty  degeneration  are  not  common 
although  occasionally  present  in  the  epithelium  of  the  tubules. 
The  pelvis  is  often  sprinkled  with  ecchymoses. 

The  bladder  may  contain  ecchymoses. 

It  is  important  to  note  that  throughout  the  kidneys,  liver 
and  spleen  pigment  may  be  more  or  less  abundant. 

In  the  digestive  tract  the  lesions  of  this  disease  consist 
largely  of  congestion  of  the  mucosa  especially  in  lines  corres- 
ponding to  the  summits  of  the  folds  of  the  mucous  membrane. 
It  is  more  marked  in  the  caecum  and  rectum  than  in  the  colon. 
The  caecum  and  less  often  the  rectum  contain  dry,  hard  fecal 
balls.  In  some  cases  in  this  system  lesions  are  not  observable. 
In  the  older  writings  much  emphasis  is  placed  on  certain 
lesions,  mostly  nodular  or  abrasions,  in  the  digestive  tract. 
Smith  has  shown,  however,  that  most  of  these  are  due  to 
animal  parasites  and  have  no  relation  to  Texas  fever. 

As  already  stated  Texas  fever  is  a  disease  of  the  blood 
and  consequently  it  is  in  this  fluid  that  the  most  constant  and 
morbid  changes  occur.  They  are  characterized  by  the  blood 
becoming  thin  and  watery  with  a  destruction  of  the  red  blood 
corpuscles.  In  some  of  the  cases  the  loss  of  corpuscles  is 
rapid  and  continuous  until  death  or  convalescence,  while 
in  others  there  is  a  marked  oscillation  between  destruction  and 
regeneration.  In  some  animals  the  loss  is  not  continuous,  but 
the  course  of  the  disease  is  marked  by  periods  of  rapid  blood 
destruction  and  periods  of  rest,  or,  as  it  were,  where  the  blood 
destruction  was  holding  its  own.     These  points  are  best  illus- 


H8 


TEXAS    FEVER 


trated  from    actual  cases   three  of  which  are   taken  from  the 
report  b}'  Smith  and  Kilborne. 


(No.  129.) 

(No. 

142.) 

(No. 

56.) 

Date. 

No.  of 
Corpuscles. 

Date 

• 

No.  of 
Corpuscles. 

Date 

No.   of 
Corpuscles^ 

Aug.  II, 

6,123,000 

Sept. 

16, 

6,890,000 

Sept. 

20, 

6,844,000 

13, 

7,171,000 

22, 

5,430,000 

22, 

5,640,000 

16, 

5,370,000 

24, 

4,562,000 

29. 

5,307,000 

27, 

3,210,000 

29. 

5,274,500 

Oct. 

9. 

5,436,000 

29- 

1,675,000 

Oct. 

4, 

3,902,000 

22, 

4,666,000 

30, 

Died  8  p.  m. 

s, 

5,983,000 

25, 

2,754,000 

22, 

4,333.000 

30, 

2,720,000 

First  hi 

gh  A.  M.  temp. 

Nov. 

4, 

5,586,000 

Nov. 

6, 

2,344,000 

Aug.  24. 

8, 
13, 

1,984,000 
1,183,000 

As  evidence  of  the  diminution  of  the  number  of  corpus- 
cles within  the  body  these  authors  point  ( i )  to  the  loss  of 
hemoglobin  through  the  kidneys,  (2)  the  over  production  of 
bile  which  is  abnormal  in  the  abundance  of  pigment  and  (3;  to 
the  actual  observation  of  their  destruction  by  the  micro-parasite 
under  the  microscope. 

The  regeneration  of  blood  corpuscles  is  indicated  perhaps- 
by  the  count,  but  more  surely  by  the  form  of  the  corpuscles 
themselves.  The  abnormal  forms  are  the  very  large  corpus- 
cles, "punctate"  forms  and  lastly  the  diffuse  stained  or 
' '  tinted  ' '  forms  and  the  hematoblasts.  The  first  of  these 
may  appear  when  the  blood  count  reaches  3,000,000  and  the 
other  forms  when  it  is  still  lower.  These  various  forms,  how- 
ever, are  probably  embryonic  or  immature  corpuscles,  which 
are  forced  prematurely  into  the  circulation  by  the  blood  pro- 
ducing organs  in  trying  to  overcome  the  rapid  destruction  of 
corpuscles  by  the  parasite.  The  action  of  the  disease  upon 
the  leucocytes  or  the  defensive  activities  of  the  white  corpuscles, 
in  combating  the  parasite  of  Texas  fever  have  not  been  deter- 
mined. In  the  work  thus  far  performed  and  reported,  they 
have  received  little  attention.  Suffice  it  to  sa}^  that  they  have 
not  been  in  evidence  in  this  conflict  and  probably  take  little  or 
no  part  in  the  morbid  changes  of  Texas  fever. 


"        ''o?I^* 


PREVENTION  249 

§  185.  Differential  diagnosis.  Texas  fever  is  easily 
differentiated  from  other  disorders  or  infectious  diseases  by  the 
presence  of  its  specific  parasite. 

In  the  absence  of  a  suitable  microscope  the  differentiation 
can  in  most  cases  be  made  from  the  character  of  the  lesions, 
the  history  of  the  animals,  the  presence  of  the  cattle  tick  and 
the  course  of  the  disease.  The  lesions  are  not  simulated  by 
any  other  disease  of  cattle,  although  the  enlarged,  dark  spleea 
may  suggest  anthrax  and  in  a  hasty  diagnosis  the  two  may  be 
confused.  From  the  fact  that  all  animals  exposed  together 
usually  come  down  with  the  disease  together  poisoning  may 
be  suggested,  but  here  again  a  study  of  the  symptoms  and 
lesions  are  sufficient  to  eliminate  toxic  disorders. 

§186.  Prevention.  The  discovery  of  the  specific  cause 
of  Texas  fever  and  of  the  cattle  tick  as  the  common  means  of  its 
transmission  has  reduced  the  preventive  measures  to  a  direct 
warfare  against  the  tick.  The  National  Government  has 
determined  the  territory  in  which  the  tick  naturally  exists  and 
from  which  cattle,  on  account  of  the  parasite,  cannot  be 
shipped  to  uninfected  districts,  except  under  certain  very 
restricted  conditions.  (See  regulations  for  transmission  of 
cattle  p.  618,  Report  of  the  Bureau  of  Animal  Industry  for 
1898.)  Likewise  susceptible  northern  cattle  cannot  be  trans- 
ported to  the  infested  districts  (south  of  Texas  fever  line) 
unless  they  can  be  placed  in  fields  that  have  been  freed  from 
ticks.  The  elimination  of  the  disease  depends  therefore,  upon 
the  elimination  of  Bo'dphilus  bovis.  While  this  may  be  im- 
possible in  the  territory  of  large  ranches,  there  seems  to  be  no 
reason  why  in  the  dairy  districts  of  the  South  it  cannot  be 
accomplished. 

^  187.  Immunizing  susceptible  cattle.  A  number 
of  investigations  have  been  undertaken  directed  toward  the 
development  of  methods  for  immunizing  northern  cattle 
against  Texas  fever  in  order  to  enable  the  shipment,  especially 
of  breeding  stock,  into  the  south.  In  1895,  the  writer  in  con- 
junction with  Dr.  E.  C.  Schroeder,  began  an  immunizing 
experiment  which  v/as  continued  and  reported  by  Dr.  Schroeder 
in  189S. 


250 


TEXAS    FEVER 


Young  animals  were  selected  and  injected  with  blood 
taken  directl_v  from  the  jugular  veins  of  southern  animals. 
The  injections  were  made  in  the  fall  and  winter  and  in  the 
spring  the  animals  were  placed  in  a  highl}'  infested  field  at 
Manchester,  Va. ,  where  they  remained  for  the  summer.  Dur- 
ing this  time  they  were  under  the  immediate  observation  of 
Dr.  Cooper  Curtice  who  made  a  careful  study  of  the  blood, 
temperature  and  extent  of  tick  invasion.  The  results  of  this 
experiment  are  shown  in  Dr.  Schroeder's  tabulation  which  is 
appended.  The  animals  were  again  exposed  the  following 
season  without  the  development  of  Texas  fever. 


Animal. 

Effect  of 

Effect  of  the  ex- 

blood injection. 

posure  to  cattle  ticks. 

I 

Severe. 

Very  mild  disease. 

2 

i  I 

Well  marked  but  mild. 

0 

Very  severe. 

Very  mild. 

4 

it                  n 

No  disease. 

5 

Mild. 

( (         (I 

6 

" 

Verv  mild. 

7 
8 

9 

Severe. 

No  disease. 

i  1 

i  i                    C  ( 

Control  Animals. 

lO 

Died,  June  20. 

II 

"      July  9- 

12 

June  26. 

13 

"      July  9- 

U 

Very  severe  disease,  recovered. 

The  inoculation  di-sease  appears  in  from  eight  to  ten  days 
after  the  injection  of  the  blood.  It  lasts  from  one  to  two 
weeks.  The  symptoms  are  occasionally  of  a  still  shorter  dura- 
tion, but  the  altered  condition  of  the  blood  persists  in  some 
cases  for  a  much  longer  period. 

Dalrymple,  Dodson  and  Morgan,  of  the  Louisana  Experi- 
ment Station,  conducted  experiments  along  this  line.  To 
show  the  results  of  their  investigations,  a  somewhat  condensed 
summary  of  their  experiments  is  given. 

Immunity  against  a  fatal  attack  of  Texas  fever  can  be 
conferred  on  susceptible  cattle  by  inoculation  with  the  blood  of 


IMMUNIZING   SUSCEPTIBLE    CATTLE  25 1 

a  native  Southern  animal    or   one  which    has    recently    been 
rendered  immune. 

When  used  in  five  cubic  centimeter  doses,  blood  from  a 
recently  immunized  animal  gave  a  less  virulent  and  less  pro- 
tracted form  of  the  artificially  produced  fever  than  a  similar 
amount  from  a  native. 

Two  and  one-half  cubic  centimeters  of  blood  from  a 
recently  immunized  animal  gave  satisfactory  results  on  two 
imported  Herford  calves,  aged  eight  and  five  months  respec- 
tively. Two  cubic  centimeters  of  the  same  blood  acted  satis- 
factorily when  injected  in  a  one-month-old  calf.  Animals  that 
had  been  allowed  sufficient  time  to  perfectly  recover  from  the 
inoculation  fever  before  being  exposed  on  a  tick-infested  pas- 
ture suffered  no  apparent  ill  effects  from  the  ticks.  Animals 
exposed  before  convalescence  was  complete  suffered  a  tempo- 
rary relapse. 

The  Experiment  Station  of  that  state  offers  to  immunize 
(free  of  charge)  northern  cattle,  if  they  are  shipped  to  the 
state,  for  its  stock  raisers 

In  Missouri,  Connaway  has  immunized  a  few  animals  with 
the  blood  serum  from  immune  (Southern)  cattle.  This 
method,  however,  needs  further  testing.  In  Mississippi, 
Robert  has  tried  the  serum  for  both  prevention  and  treatment 
with  somewhat  similar  results.  In  Virginia  and  Oklahoma 
the  disease  and  its  prevention  have  been  studied.  In  Texas, 
Francis  has  conducted  a  number  of  immunizing  experiments 
with  most  excellent  results.  He  has  pointed  out  the  value  of 
immunizing  young  (2  to  6  weeks  old)  calves  by  artificially  in- 
festing with  ticks.  In  Australia  the  problem  of  immunizing 
cattle  against  the  effects  of  the  spreading  of  the  cattle  tick  in 
order  to  save  their  stock  from  "tick  fever"  has  become  a  matter 
of  serious  consideration. 

The  very  limited  knowledge  of  the  life  cycle  of  the  para- 
site of  Texas  fever  precludes  a  satisfactory  explanation  of  the 
modus  operandi  in  the  production  of  immunity  by  these  various 
procedures.  On  this  point  there  is  need  for  much  extended 
investigation. 


252  INFECTIOUS    ENTERO-HEPATITIS 

REFERENCES. 

1.  Babes.  Die  Aetiologie  der  seuchenhaften  Haenioglobinurie  des 
Rindes.      Virchow's  Archiv.     Jan.  1889. 

2.  CONNAWAV.  Texas  fever  or  acclimation  fever.  Bjilletiii  No. 
J  J.     Mo.  State  Board  of  Agriculture.     1897. 

3.  Dai.rvmple,  Morgan  and  Dodson.  Texas  or  southern  cattle 
fever.     Bulletin  ^i.     Louisiana  Agric.  Exp.  Station.    189S. 

4.  DiNWiDDiE.  Some  Texas  fever  experiments.  Bulletiti  No.  20. 
Ark.  Agric.  Exp.  Station.      1893. 

5.  Francis  and  Connaway.  Texas  fever.  Bulletin  No.  jj. 
Texas  Agric.  Expt.  Station.     1899. 

6.  Gamgee,  Dodge,  Billings  and  Curtis.  Diseases  of  Cattle  in 
the  United  States.  Report  of  the  commissioner  of  agriculture,  Washing- 
ton, D.  C.     1871. 

7.  Hunt  and  Collins.  Report  on  tick  fever.  Brisbane.  Queens- 
land, Australia,  1896. 

8.  Lewis.  Texas  fever.  Bulletin  No.  jp.  Oklahoma  Agric. 
Expt.  Station.     1899. 

9.  IviGNiijRES.  Da  "Tristeza"ou  Malaria  Bovine  dans  la  Repub- 
lique  Argentine.     Buenos  Aires.      1890.      ( Full  bibliograph}-). 

ID.  Mayo.  Texas  Fever.  Bulletin  No.  6g.  Kan.  Agric.  Exper. 
Station.      1897. 

11.  McCuLLOCH.  The  prevention  of  Texas  fever  and  the  amended 
laws  controlling  contagious  diseases.  Bulletin  No.  104.  l^iiginia  Agi'ic. 
Expt.  Station.     1899. 

12.  NiLES.  Splenetic  or  Texas  cattle  fever.  Bulletin  A^o.  61. 
Virginia  Agr.  Expt.  Station.     1896. 

13.  NoRGA.\RD.  Dipping  cattle  for  the  destruction  of  ticks. 
Annual  Report,  Bureau  of  Animal  Industry.     1895-6.     p.  109. 

14.  Paouin.  Texas  fever.  Bidletin  No.  11 .  I\Io.  Agric.  Exp. 
Station.     1890. 

15.  Salmon.  Contagious  diseases  of  animals.  Special  report  A^o. 
22.      Washington,  D.  C. 

16.  S-A.LMON.     Report  Commissioner  of  Agriculture.     1881-2. 

17.  S.^LMON.    Annual  Reports,  Bu7'eau  of  Animal  Industry.   1884-5. 

18.  SCHROEDER.  Inoculation  to  produce  immunity  from  Texas 
fever  in  Northern  cattle.     Ibid.      1S98.     p.  273. 

19.  Smith.  Preliminary  observations  on  the  microorganism  of 
Texas  fever.      The  Rledical  Nezus.     Dec.  21,  1889. 

20.  Smith  and  Kilborne.  Texas  fever.  Bulletin  No.  i. 
Bureau  of  Animal  Industry.     U.  S.  Dept.  Agriculture.     1893. 

21.  Smith  and  Kilborne.  Aniiual  Report,  Bureau  of  Animal 
Industry.      1891-2.    (Issued  iSg^). 

22.  Stiles.     Report  New  York  State  Board  0/ Health.     186S. 


INFECTIOUS  ENTERO-HEPATITIS  IN  TURKEYS. 

§  188.  Characterization.  This  disease  of  turkeys  is 
characterized  by  thickening  of  areas  or  of  the  entire  walls  of 
the  caeca  and  areas  of  tissue  degeneration  or  necrosis  in  the 
liver.     It  is  popularly  known  as  "black  head." 


GEOGRAPHICAL    DISTRIBUTION  253 

§  189.  History.  In  the  fall  of  1893,  Prof.  Samuel 
Cushman  of  the  Rhode  Island  State  Experiment  Station  sent 
a  few  specimens  of  the  diseased  organs  of  turkeys  which  had 
died  of  "black  head"  to  the  Bureau  of  Animal  Industry  where 
they  were  carefully  examined  by  Dr.  Theobald  Smith.  In  the 
summer  of  1S94,  Dr.  Smith  made  a  careful  study  of  this 
disease  at  the  Rhode  Island  Experiment  Station.  He  found 
that  it  was  caused  by  one  of  theprotozoon  (Amoeba  meleagridis 
Smith)  and  he  published  a  full  description  of  the  disease 
which,  in  accordance  with  the  lesions,  he  designated  InfedioiLs 
en  tero-  hepatitis. 

In  1895,  the  disease  was  further  investigated  respecting 
the  mode  of  transmission  of  the  infecting  protozoa.  The 
results  showed  that  it  could  be  transmitted  directly  from 
diseased  to  healthy  turkeys  without  the  intervention  of  an 
intermediate  host.  These  results  were  published  in  1896. 
Recentl}',  Chester  of  the  Delaware  Agricultural  Experiment 
Station  has  shown  that  a  very  similar  disease  attacks  chickens. 
The  place  and  the  time  of  the  first  appearance  of  this  disease 
are  not  clearly  stated,  but  it  seems  that  New  England  was  the 
first  to  suffer  from  it. 

§  190.  Geographical  distribution.  The  available  data 
bearing  upon  the  geographical  distribution  of  this  disease 
indicate  that  it  is  widely  distributed.  The  New  England 
states,  particularly  Rhode  Island,  and  certain  districts  in  the 
middle  and  western  states  are  affected.  It  has  not  yet  been 
reported  from  the  southern  states.  For  want  of  statistics  the 
amount  of  loss  to  the  poultry  industry  occasioned  by  this 
disease  can  not  be  accurately  estimated,  but  the  fact  that  it 
has  caused  many  farmers  and  poultry  men  in  New  England  to 
discontinue  the  raising  of  turkeys  shows  that  it  is  of  much 
economic  importance.  It  is  stated  in  the  report  of  the  Rhode 
Island  Experiment  Station  for  1894  that  "the  eradication  of 
this  disease  would  be  worth  hundreds  of  thousands  of  dollars 
to  the  eastern  farmers  alone."  These  heavy  losses  in  the  east, 
together  with  the  accumulating  evidence  that  the  entire 
northern  third  of  this  country  is  sprinkled  with  infected  dis- 
tricts from  which  the  disease  is  spreading,  indicate  that  this 


254 


INFECTIOUS    ENTERO-HEPATITIS 


maladv  is  of  more  than  ordinary  sienificance  to  those  ensraeed 

-CD  O       O 

in  the  turkey  industry. 

§  191.  Etiology.  In  1895,  Smith  described  a  micro- 
organism belonging  to  the  protozoa  which  he  found  to  be 
associated  directly  with  the  disease  process.  He  designated  it 
Amcvba  meleagridis.  In  those  cases  in  which  the  disease  was 
recent,  or  at  its  height,  the  parasites  were  very  numerous  in 
the  affected  tissues,  while  in  those  in  which  the  disease  process 
was  far  advanced  and  associated  with  degenerative  or  regen- 
erative changes,  the  parasites  were  found  with  difficulty. 

The  most  fre- 
quent appearance  pre- 
.sented  by  the  para- 
sites is  that  of  round 
homogeneous  bodies 
with  a  sharply  de- 
fined, single-con- 
toured outline.  With- 
in these  bodies  and 
situated  some  what 
eccentric  ally  is  a 
group  of  very  minute 
granules,  probably 
representing  a  nuclear 

structure.    Thev  vary 

,  .      '      .  Fig.  63.     Ama-ba  meleagridis.     (/)  Iso- 

somewhat     lusize,,.  1  \     ■     i     j.        u       ,^ 

latea   organisms ;   {2)   single    parasites;  (j) 

measuring    ironi    8    to    groups  {a)  of  the  amoebcs  in  mucous  membrane 

\0)x    in    diameter    in    of  a  turkey's  ccscum.     (Smith). 

some  cases,  from  12  to  14//  in  others.  In  the  fresh  tissues 
they  are  distinctl)-  larger  than  the  parasites  within  the  tissues, 
which  have  undergone  the  hardening  process.  The  latter  are 
from  6  to  10/^  in  diameter.  This  difference  ma}-  be  due  to 
shrinkage,  on  the  one  hand,  and  on  the  other  to  a  slight  flat- 
tening of  the  bodies  by  pressure  in  the  fresh  preparations. 
These  peculiar  homogeneous  bodies  were  found,  as  a  rule,  free 
in  the  crushed  preparations,  although  occasionally  giant  cells 
were  detected  which  contained  a  number  of  them.  The  cell 
nuclei  of  the  giant  cells  are  not  visible  in  the  fresh  condition. 


ETIOLOGY  255 

Numerous  coarse   granules,  less    frequently   fat    globules,  are 
embedded  in  its  protoplasm. 

Smith  believed  from  the  results  of  his  investigations  that 
the  parasite  lived  in  the  interstices  and  lymph  spaces  of  the 
tissue,  but  not  within  cells.  This  seems  certainly  true  of  the 
ctecum.  In  the  liver,  the  liver  cells  seem  to  become  necrotic 
or  else  disappear  so  rapidly  that  it  is  impossible  to  determine 
just  where  the  parasites  begin  to  multiply.  They  do  not  live 
within  the  blood  vessels,  as  they  are  not  found  within  them 
excepting  perhaps  in  a  thrombosed  vessel.  They  must,  there- 
fore, occupy  the  place  of  the  liver  cells.  It  is  probable  that 
they  begin  to  multiply  in  the  connective  tissue  adjoining  the 
blood  vessel  and  simply  crowd  out  the  liver  cells,  leaving  the 
connective  tissue  stroma  of  the  lobules  in  whose  meshes  they 
are  found. 

Their  presence  within  giant  cells  is  seen  in  almost  every 
infected  organ  subject  to  examination.  In  teased  preparations 
of  the  fresh  tissues  they  are  frequently  found  with  remnants  of 
the  inclosing  cells  still  attached.  This  intracellular  condition 
is,  however,  a  purely  passive  one  so  far  as  the  parasite  is 
concerned. 

The  raicroparasites  within  the  tissues  of  the  host  seem  to 
tend  toward  destruction.  Both  the  death  of  the  tissue  itself 
and  the  repair  seem  to  lead  to  the  disappearance  of  the  para- 
sites. In  most  cases  there  may  be  seen  in  the  same  section 
a  partial  dissolution  of  some  of  the  bodies,  while  others  are 
still  in  good  preservation.  Evidently  their  life  within  the 
tissues  is  not  very  long. 

A  discharge  of  the  microparasites  which  escape  destruc- 
tion probably  takes  place  from  the  walls  of  the  caeca,  when 
these  break  down  into  the  contents  with  which  they  are  carried 
outward.  A  similar  discharge  may  take  place  from  the  liver 
through  the  bile  ducts  into  the  intestine.  Anpther  way  of 
dissemination  is  in  the  death  of  the  diseased  turkey  and  the  dis- 
solution of  its  body  whereby  the  organisms  are  set  free.  The 
occurrence  of  amoebae  in  intestinal  affections  of  man  was  noticed 
by  Losch  in  1875.  Since  that  time  it  has  been  the  subject  of 
many  investigations. 


256  INFECTIOUS  ENTERO-HEPATITIS 

The  points  of  analogy  between  the  avian  and  the  human 
disease  are  that  in  both  there  is  an  affection  of  the  intestine 
(large  intestine  in  man,  caeca  in  turkeys)  associated  with  liver 
disease  due  to  amoebae. 

The  intestinal  wall  in  amoebic  dysentery  is  greatly  thick- 
ened, owing  to  an  oedematous  condition.  It  is  also  thickened 
in  circumscribed  areas  and  contains  cavities  filled  with  gela- 
tinous-looking pus.  The  amoebae  vary  much  in  size  and  con- 
tain vacuoles.  They  are  found  in  variable  numbers  in  the 
.bottom  of  the  ulcers  and  in  the  discharges.  The  large  num- 
bers of  amoebae  found  in  the  intestinal  contents  led  Council- 
man and  Lafieur  to  infer  an  active  multiplication  therein. 
The  presence  of  the  parasites  within  the  submucosa  is 
described  by  these  authors  in  one  case  only. 

In  the  turkey,  the  parasites  are  always  present  in  the  con- 
nective tissue  spaces  of  the  mucous  and  submucous  mem- 
brane. Their  presence  in  the  contents  of  the  caecum  is  highlj^ 
probable. 

It  differs  from  the  Ainceba  dysenterice  in  being  quite  uni- 
form in  its  appearance,  varying  but  slightly  in  size  (from  6  to 
10//  in  diameter)  and  in  being  free  from  vacuoles.  Movements 
characterized  as  amoeboid  have  not  yet  been  demonstrated. 

The  liver  affection  in  man  appears  usually  as  an  abscess. 
In  turkeys  it  appears  as  a  variable  number  of  foci  in  which 
the  microparasites  may  be  present  in  great  abundance.  The 
difference  in  the  nature  of  the  lesions  must  be  largely  attri- 
buted to  the  different  reaction  of  the  tissues  of  birds  toward 
injuries. 

§  192.  Symptoms.  Diarrhoea  is  the  symptom  which 
sooner  or  later  may  be  expected  to  appear.  It  probably 
occupies  the  most  prominent  place  among  the  objective  mani- 
festations. The  disease  of  the  caeca  is  presumably  responsible 
for  this.  Diarrhoea  occurs  with  at  least  one  other  disease  of 
the  caeca  and  with  the  presence  of  tapeworms.  Emaciation  is 
pronounced  in  very  chronic  cases  but  it  is  not  constantly  pres- 
ent. As  it  may  accompany  other  wasting  diseases,  it  can  not 
be  depended  upon  as  an  indication  of  this  affection.  As  the 
disease  progresses  the  turkeys  become  less  active,  hang  behind 


MORBID  ANATOMY  257 

their  flock  or  do  not  go  out  with  it.  Later  the  comb,  wattles 
and  even  the  skin  of  the  head  become  dark  colored,  hence  the 
popular  name  "black-head." 

§  193.  Morbid  anatomy.  Turkeys  are  attacked  quite 
young.  Smith  tbund  a  turkey  about  three  weeks  old  in  which 
the  disease  had  already  made  considerable  progress.  It  seems, 
moreover,  as  if  the  disea.se  was  contracted  only  by  the  young, 
because  in  the  examination  of  turkeys  of  different  ages  the 
oldest  show  lesions  of  the  longest  standing  ;  that  is,  such  as 
had  undergone  the  most  extensive  transformation.  In  general 
it  may  be  said  that  the  age  of  the  turkey  corresponds  with  the 
age  of  the  disease  process.  The  most  serious  and  extensive 
destruction  of  tissue  occurs  in  the  turkeys  in  fall.  In  mid- 
summer the  disease  is  making  most  progress  and  the  micro- 
parasites  are  present  in  gi eater  nun.bers.  It  is  probable  that 
the  delicate  tissues  of  the  young  are  best  adapted  for  the  tem- 
porary habitat  and  rapid  multiplication  of  this  parasite.* 

The  primary  seat  of  the  disease  is  the  caeca.  From  these 
the  liver  is  secondarily  invaded.  Other  organs  have  not  been 
found  to  be  attacked. 

The  lesions  of  the  caeca  are  in  substance  a  thickening 
of  the  wall,  followed  in  most  cases  b}-  a  destruction  of  the 
epithelium  and  deeper  portions  of  the  mucous  membrane.  This 
destruction  results  in  the  outpouring  of  a  coagulable  fluid  into 
the  tube.  The  thickening  of  the  wall  may  vary  considerably 
in  extent  from  case  to  case.  It  may  be  uniform  over  the 
greater  portion  of  the  tube  or  it  may  be  limited  to  circum- 
scribed patches.  The  commonest  seat  of  these  lesionsis  near 
the  blind  end  of  the  tube  where  it  evidently  starts  and  whence 
it  spreads  to  other  portions.  Not  infrequently  only  one  cae- 
cum is  diseased,  the  other  remaining  normal. 

The  affection  of  the  caecum  is  due  primarily  to  the  multi- 
plication of  the  microorganism  which  may  take  place  chiefly 
either  in  the  mucous  membrane,  or  in  the  submucous  tissue, 
it  may,  though   rarely,  extend  into    the  muscular  coat.     The 


*In  this  regard  it  simply  follows  the  rule  observed  by  large  numbers 
■of  parasites  whose  most  destructive  action  is  visited  upon  the  young. 


2.S8 


INFECTIOUS    ENTERO-HEPATITIS 


thickening  of  the  wall  is  the  result  of 
several  processes — the  multiplication 
of  the  parasites,  the  increase  of  the 
normal  tissue  elements  and  later  on 
the  accumulation  of  masses  of  small 
cells  and  some  giant  cells. 

In  the  early  stages  of  the  inva- 
sion, the  adenoid  tissue  between  the 
tubules  and  in  the  submucosa  be- 
comes greath'  increased  owing  to  the 
presence  of  large  numbers  of  micro- 
parasites  of  round  or  slightly  oval 
outline  and  from  6  to  io/<  in  diam- 
eter which  stimulate  the  proliferation 
of  the  tissue  cells.  Numerous  mitoses 
have  been  seen  in  this  stage.  The 
parasites  seem  to  occupy  the  meshes 
of  the  adenoid  tissue  either  singly 
or  in  groups  or  nests.  In  these 
meshes  they  are  soon  enveloped  in 
cells  acting  as  phagocytes,  so  that  the 
appearance  of  an  intracellular  habitat 
of  the  parasites  is  suggested. 

The  presence  of  the  parasites  in 
this  reticulum  probably  stimulates  also 
the  accumulation  of  lymph  cells  with- 
in the  spaces,  in  virtue  of  which  the 
mucous  membrane  is  thickened.  In 
this  early  stage  of  invasion  the  epi- 
thelium, both  of  the  tubules  and  of  the  surface,  remains  unaf- 
fected. The  parasites  do  not  invade  the  epithelium  at  any  time. 
As  the  disease  progresses  there  is  a  continued  increase  in 
cellular  elements  of  the  mucous  and  submucous  coats  and  a 
gradual  invasion  of  the  muscular  coats.  Here  the  bundles  of 
fibers  of  the  circular  coat  are  thrust  apart  by  masses  of  cells, 
so  that  this  coat  also  becomes  greatly  thickened.  The  inflam- 
mation finally  extends  to  the  serous  covering,  where  the  blood 
vessels  become  greatly  dilated  and  give  the  caecum  a  congested 


Fig.  64.  Caeca;  a 
and  b  are  diseased  areas  ; 
c,  section  of  thickened 
ivall. 


MORBID   ANATOMY 


259 


appearance.  In  cases  of  ordinary  severity  the  wall  of  the 
caecum  which  is  not  more  than  0.2  to  0.5  mm.  thick  normally 
becomes  2  to  ^  mm.  thick. 


1 


.^- 


% 


lif 


With  the  progress  of  the 
disease  the  mucous  membrane  may 
be  shed  and  a  coagulable  fluid 
poured  out  into  the  caecum.  In 
some  cases  it  appears  in  isolated 
masses,  which  adhere  to  certain 
spots  of  the  mucous  membrane.  In 
others,  this  exudate  fills  the  entire 
tube  with  a  yellowish-white  mass, 
built  up  in  concentric  layers  con- 
sisting of  a  mixture  of  blood  cor- 
puscles, fibrin  and  small  round  cells 
in  variable  proportion. 

In  the  further  progress  of  the 
local  disease  it  is  not  improbable 
that  bacteria  are  also  concerned. 
The  exudate  contains  immense 
numbers  of  them  and  the  denuded 
mucosa  furnishes  a  favorable  place 
of  entry.  It  is  otherwise  difficult 
to  explain  the  continued  increase  in 
thickness  of  the  walls  of  the  caecum 
after  the  mucous  membrane  has 
been  shed.  This  continued  increase 
in  thickness  is  due  to  an  extensive 
infiltration  of  small  round  cells  and 
the  presence  of  some  giant  cells. 
Parasites  in  this  advanced  stage  are 
scarce     and     usually    recognizable 

-only  as  vacuole-like  bodies  within    showing    thickvess    of    wall 
the  <yiant  cells.  a^id  ulcerated  wucosa. 

The  thickening  of  the  wall  is  associated  in  some  cases 
with  an  extension  of  the  inflammation  to  the  contiguous  wall 
of  the  intestine  which  becomes  firmly  attached  to  the  caecum. 


Fig.  65.  Diseased  caecum 


26o 


INFECTIOUS    ENTERO-HEPATITIS 


Yellowish  exudates  are  sometimes  found  outside  of  the  diseased 
caecum  on  its  serous  covering  and  the}-  bind  it  inextricably  ta 
the  other  caecum  or  to  the  intestine  or  attach  it  to  the  abdomi- 
nal wall.  In  these  stages,  the'niicroparasite  is  not  found.  It 
seems  to  have  done  its  work  by  destroying  the  mucous  mem- 
brane and  to  have  left  the  field  for  miscellaneous  bacteria. 

Other  portions 
of  the  digestive 
tract  are  not  affect- 
ed. The  secondary 
lesions  are  found  in 
the  liver  although 
in  some  cases  they 
do  not  appear.  The 
organ  itself  is  en- 
larged to  probably 
twice  the  normal 
size.  Over  the  sur- 
face are  distributed 
roundish,  d  i  sco  1- 
ored  spots,  dis- 
tinctly demarcated 
from  the  surround- 
ing tissue.  These  may  be  distributed  uniformly  over  the  whole 
surface  of  the  liver  or  they  ma}-  be  limited  in  number  to  a  few. 
They  vary  from  3  to  15  mm.  in  diameter.  Several  types  of 
these  spots  appear  corresponding  to  different  conditions  of  the 
diseased  tissue.  We  have  in  the  early,  most  active  disease 
process  sharply  defined  circular  areas  of  a  lemon  yellow,  of  a 
neutral  gray  or  of  an  ochre  yellow  color.  The  spot  is  not  homo- 
geneous in  structure,  but  made  up  of  a  delicate  network  of 
grayish  yellow,  dead  tissue. 

In  another  class  of  spots  there  is  a  mottled  brownish  color 
which  contrasts  only  slightly  with  the  surrounding  liver  tissue 
by  its  darker  color.  It  may  contain  a  central  yellow  nucleus 
of  dead  tissue  and  a  narrow  outer  border  of  the  same  character, 
or  the  border  may  be  a  dark  brownish  circular  line.  The  entire 
spot   has   an   indistinct  appearance    and  is   flattened   or  even 


Fig.  66.     Liver  showing  diseased  foci. 


MORBID    ANATOMY  26 1 

slightly  depressed  below  the  surface.  In  some  cases  they  are 
uniformly  whitish  and  shade  off  somewhat  gradually  into  the 
surrounding  tissue.  In  sections  of  the  affected  organ  it  will  be 
found  that  the  surface  spots  represent  masses  of  liver  tissue  in 
the  same  condition,  the  spots  being  simply  the  places  where 
these  diseased  foci  intersect  the  surface.  Some  are  found 
deeply  imbedded  in  the  liver  tissue,  and  therefore  not  visible 
on  the  surface.  The  lesion  of  the  liver  is  thus  represented  by 
few  or  many  foci  of  disease  having  in  general  a  spherical  form 
and  appearing  on  the  surface  of  the  organ  as  round  spots. 
Occasionally  the  lesions  become  more  extensive  and  the  death 
of  large  Dortions  of  liver  tissue  follows. 

o  J. 

The  changes  in  the  liver  are  most  easily  explained  by 
assuming  that  the  microparasites  are  conveyed  by  the  blood 
directly  from  the  diseased  caeca  into  the  liver  and  there  de- 
posited in  different  places,  where  they  begin  to  multiply  and 
spread  in  all  directions.  In  this  way  they  form  the  spherical 
foci  of  disease  which  appear  as  circles  on  the  surface  of  the 
liver.  This  theory  is  borne  out  by  the  results  of  the  micro- 
scopic examination. 

In  sections  of  hardened  tissue  from  the  liver  in  which  the 
disease  has  but  recently  begun,  the  affected  regions  are  invaded 
by  large  numbers  of  protozoa  which  occupy  a  kind  of  reticu- 
lum formed  probably  from  the  connective  tissue  stroma.  The 
liver  cells  have  partially  or  wholly  disappeared  from  these  foci. 
The  parasites  occupy  the  meshes  of  the  tissue  either  singly  or 
in  groups.  The  reticulum  is  provided  with  a  small  number  of 
nuclei,  some  of  which  are  closely  applied  to  and  curved  partly 
around  the  parasite.  The  blood  vessels  are  usually  much 
dilated  and  filled  with  red  corpuscles. 

The  yellow  masses  observed  with  the  naked  eye  in  the 
surface  spots  are  shown  to  be  patches  of  an  amorphous  sub- 
stance which  take  nuclear  stains  very  feebly,  the  aniline  colors 
not  at  all.  It  may  be  described  as  a  coarse  network  in  the 
meshes  of  which  small  cells,  and  very  rarely  parasites,  are 
seen.  This  substance  is  assumed  to  be  the  result  of  coagula- 
tion necrosis  of  the  liver  cells  by  which  they  have  lost  their 
nuclei  and  have  become  fused  into  a  formless  mass.       It    is 


262  INFECTIOUS    ENTERO-HEPATITIS 

probable  that  the  plugging  of  blood  vessels  in  the  liver  by 
parasites  carried  from  the  caecum  is  the  cause  of  the  necrosis, 
since  such  plugs  or  thrombi  are  not  uncommon  in  sections  of 
the  diseased  spots. 

With  the  appearance  of  the  microparasites  reactive 
changes  begin  at  once  which  complicate  the  process.  We 
have  at  the  outset  an  active  multiplication  of  the  micropara- 
sites which  takes  the  place  of  the  original  liver  tissue  and  a 
process  of  coagulation  necrosis  going  on  at  the  same  time. 
Soon  multinucleated  (or  giant)  cells  appear  which  not  only 
take  in  the  microparasites  but  which  are  also  engaged  in 
removing  dead  tissue.  At  least  their  collection  in  groups 
around  and  within  the  necrotic  areas  leads  to  this  assumption. 
Not  infrequently  they  are  grouped  around  what  appears  to  be 
a  plugged  vessel  or  else  they  occupy  the  lumen  of  the  vessel 
itself. 

In  still  older  cases  the  diseased  areas  are  found  more  or 
less  filled  with  small  round  cells  which  maj'  have  passed  into 
the  dead  regions  from  the  blood  vessels.  In  all  cases  the  latter 
are  more  or  less  enlarged  and  they  seem  to  encroach  upon  the 
liver  tissue,  thus  filling  in  part  the  void  produced  by  the  cell 
death  and  giving  the  surface  of  the  liver  a  brownish,  mottled 
appearance  wherever  the  disease  spots  are.  The  processes  of 
advancing  disease  and  necrosis  or  death  of  tissue  on  the  one 
hand  and  of  repair  on  the  other  seem  to  go  on  side  by  side, 
now  one  now  the  other  predominating. 

The  results  of  the  investigations  thus  far  made  indicate 
that  the  disease  may  follow  several  courses,  viz. : 

(i )  After  a  certain  period  of  disease  regenerative  processes 
begin  which  tend  toward  a  permanent  recovery. 

(2)  The  disease  may  proceed  so  rapidly  from  the  very 
start  that  the  affected  turkeys  die  early  in  life. 

(3)  The  disease  may  come  to  a  standstill  but  the  amount 
of  dead  tissue  in  the  caeca  and  liver  may  be  so  great  as  to 
favor  the  entrance  of  bacteria  which  are  directly  responsible 
for  the  death  of  the  bird  late  in  the  summer  or  fall. 

The  description  of  the  lesions  of  a  turkey  dead  of  this 
disease  is  appended.      It  is  quoted  from  Smith's  report. 


MORBID    ANATOMY  263 

Turkey  No.  /^.— About  3  months  old.  Taken  from  a  flock  August 
8  because  of  lack  of  strength  to  keep  up  with  the  rest  when  driven. 
Indications  of  diarrhoea.  Placed  in  a  coop,  where  it  died  during  the 
night.     Examined  next  morning. 

Slight  odor  of  decomposition.     A  few  small  warts  on  skin  of  neck. 
The  various  organs  were  found  normal,  with  the  following  exceptions  : 
Mucosa  of  duodenum  almost  blackish,  from  intense  injection  and 
pigmentation  of  villi. 

Both  caeca  diseased.  The  left  is  slightly  distended.  On  serous 
aspect  two  yellowish  spots,  with  markedly  injected  borders,  correspond- 
ing to  thickenings  of  the  walls  near  the  blind  end  of  tube.  The  mucous 
surface  of  one  is  smooth  ;  to  the  other  an  exudate  is  attached.  Besides 
the  thickening  at  these  spots,  the  free  half  of  this  caecum  is  somewhat 
thickened  uniformly. 

The  right  caecum  is  very  much  distended  over  two-thirds  of  its 
length.  From  the  serous  surface  local  thickenings  are  recognizable, 
which  have  a  yellowish,  mottled  appearance.  The  small  intestine  is 
firmly  attached  to  one  of  these.  The  disease  has,  however,  not  invaded 
the  wall  of  the  latter.  The  border  of  these  spots  is  intensely  hyperaemic. 
AVhen  the  caecum  is  slit  open  its  width  is  three  to  four  times  that  of  the 
undistended  tube,  and  the  thickness  of  the  wall  varies  from  one-eighth 
to  one-half  of  an  inch,  being  not  less  than  one-eighth  of  an  inch  over 
three-fourths  of  the  entire  length.  When  the  brownish  feces  were 
washed  away  the  increased  local  thickenings  were  found  covered  with 
firm  exudates,  usually  attached  in  but  one  spot. 

Sections  were  examined  of  that  portion  of  the  caecal  walls  which 
was  very  nmch  thickened,  and  to  which  the  contiguous  small  intestine 
was  inseparately  attached  by  the  new  growth. 

The  mucosa  of  the  caecal  portion  had  sloughed  away,  while  that  of 
the  embedded  small  intestine  was  intact.  The  neoplastic  tissue  between 
caecum  and  intestine  was  fully  i  cm.  (two-fifths  inch)  thick.  Inasmuch 
as  the  infiltration  probably  followed  the  narrow  mesentery  between 
caecum  and  intestine  the  original  boundary  lines  of  the  caecal  wall  are 
no  longer  recognizable.  The  muscular  coat  of  the  caecum  may  be  traced 
for  only  a  short  distance  into  the  neoplasm,  when  it  disappears.  Micro- 
parasites  were  not  seen  distinctly  in  the  diseased  tissue. 

The  liver  is  very  much  enlarged,  and  dotted  everywhere  with 
roundish  spots  of  varying  appearance.  The  majority  are  from  5  to 
12  mm.  in  diameter,  round  or  slightly  oval.  The  center  of  each  is 
usually  occupied  by  a  group  of  yellowish  dots  and  the  circle  is  bounded 
bv  a  narrow  yellowish  ring.  The  space  of  the  circle  is  mottled  brownish. 
Among  these  spots  there  are  also  circles  of  a  completely  yellowish  color. 
On  the  convex  surface  of  the  left  lobe  there  is  a  very  firm,  ring-like, 
yellowish  mass,  cutting  like  firm  cheese. 

In  crushed  preparations  of  fresh  liver  tissue  from  within  the  brown- 
ish circles  many  giant  cells  are  seen.     They  consist  of  a  meshwork  of 


264  INFECTIOUS   ENTERO-HEPATITIS 

protoplasm  of  a  rather  coarsely  granular  character  inclosing  spheres 
which  appear  homogeneous.  The  giant  cells  are  up  to  30//  in  diameter. 
Sections  of  liver  tissue  hardened  in  alcohol  and  in  Foa's  solution 
were  also  examined.  The  foci  of  disease  contain  necrotic  areas  in  which 
are  numerous  giant  cells  each  inclosing  a  number  of  microparasites.  In 
some  portions  there  is  much  cell  infiltration  in  the  interlobular  tissue 
around  the  portal  vessels.    Among  the  cells  the  protozoa  are  recognizable. 

§  194.  DifTerential  diagnosis.  This  disease  is  to  be 
differentiated  from  certain  local  affections  of  the  caecum  not 
especially  uncommon  in  turkeys.  Ziirn  (Deutsche  Zeit.  f. 
Thiermed,  X  (1883).  p.  189)  has  described  a  csecal  disease  in 
water  fowls  and  turkeys  and  Von  Ratz  has  described  a  caecal 
disease  in  turkeys  in  which  the  liver  lesions  seem  to  be  absent. 
The  lesions  in  the  liver  and  the  presence  of  the  microparasite, 
as  previously  described,  are  sufficient  to  differentiate  this 
disease. 

§  195.  Prevention.  The  present  knowledge  of  this 
disease  shows  that  the  parasite  is  transmitted  directly  from 
diseased  to  healthy  turkeys.  This  suggests  that  the  first  pre- 
caution is  to  avoid  the  entrance  of  diseased  or  seemingly 
healthy  turkeys  from  a  diseased  flock  into  a  healthy  one. 
The  discovery  of  Chester  indicates  that  a  like  precaution  must 
be  taken  with  reference  to  fowls.  If  the  disease  exists  the  best 
though  most  radical  method  as  suggested  by  Smith  is  the  total 
destruction  of  the  affected  flock,  thorough  disinfection  and  the 
iritroduction  of  healthy  turkeys. 

REFERENCES. 

1.  Chester.    Report  of  the  bacteriologist  of  the  Del.  College  Agric. 
Exp.  Station.      1899-1900.    (C.  reports  disease  in  chickens). 

2.  CuSHMAN.     Nature  of  black  head  in  turkeys.     Report  R.  Island 
Agric.  Exp.  Station.     1894.     p.  199. 

3.  Moore.     The  direct  transmission  of  infectious  entero-hepatitis 
in  turkeys.     Circular  No.  5,  U.  S.  Bureau  of  Aniinal  Industry.     1896. 

4.  Smith.     Infectious  entero-hepatitis  in  turkeys.     Bulletin  No.  S,, 
U.  S.  Bureau  of  Animal  Industry.     1895. 


INFECTIOUS    DISEASES  265 

SURRA. 

Synonyms.  Relapsing  fever  of  equines  ;  pernicious  anae- 
mia of  horses. 

§  ig6.  Characterization.  Surra  is  an  infectious  disease 
of  solipeds  and  camels  caused  by  a  flagellate  protozoon.  It  is 
determined  by  a  continuous  fever  with  alternate  paroxysms 
and  intermissions,  with  a  general  or  localized  eruption  of  the 
skin,  petechiae  of  the  mucosae  and  more  or  less  subcutaneous 
oedema.  There  is  rapid  emaciation  and  great  weakness.  It  is 
usually  fatal.  It  attacks  horses,  asses,  mules,  goats,  dogs, 
cattle  and  rats.  It  can  be  inoculated  into  other  animals  such 
as  rabbits  and  guinea  pigs.  From  an  economic  point  of  view  it 
is  reported  to  be  essentially  a  disease  of  horses. 

§  197.  History.  This  disease  appears  to  have  been  known 
for  many  years  to  the  natives  of  the  low  lands  on  both  sides  of 
the  Indus  on  the  northwest  frontier  of  India.  Haig  appears  to 
have  observed  it  in  Persia  in  1876.  In  1880,  Evans  found  sev- 
eral cases  of  it  in  the  Dera  Ismael  Khan  country.  He  was  the 
first  to  describe  it  and  attribute  its  cause  to  an  animal  parasite 
which  he  discovered  in  the  blood.  In  1885,  Steel  met  with  a 
disease  among  mules  in  Burma  which  he  regarded  as  identical 
with  Evan's  surra,  and  which  he  believed  to  be  relapsing  fever. 
In  1888  there  was  an  outbreak  among  the  Bombay  Tramway 
Company's  horses.  Since  then  surra  has  become  epizootic  in 
Bombay.  Lingard  reports  that  thousands  of  ponies,  horses, 
camels  and  asses  died  from  it  during  the  rains  of  1893  and 
1894.  Its  ravages  in  the  Punjab  and  Northwest  Provinces 
during  1S95  are  reported  to  be  appalling. 

§  ig8.  Geographical  distribution.  It  is  a  disease  of 
Asia  and  Africa.  It  is  reported  that  "the  .distribution  of  this 
malady  seems  to  be  entirely  influenced  by  the  physical  aspect 
of  the  country  ;  being  far  more  prevalent  in  those  parts  where 
floods  and  inundations  occur  than  in  the  higher  and  dryer 
portions"  (Pease).  If  the  identity  of  surra  with  the  t.se-tse 
fly  disease  is  accepted,  as  it  seems  to  be,  it  has  a  wide  dis- 
tribution in  Central  Africa.     • 

Surra  does  not  exist  in  the  United  States,  but  because  of 
its  prevalence  and  long  standing  in  the  Philippines  it  is  liable 


266 


SURRA 


to  be  introduced  into  this  countr}-.  For  this  reason  its  nature 
should  be  understood  b}-  American  veterinarians  and  pathol- 
ogists. 

§  199.  Etiology  There 
is  little  or  no  doubt  that  surra 
is  due  to  the  presence  in  the 
blood  of  a  flagellated  infu- 
sorian,  Tiypanosouia  Evansi. 
This  organism  is  invariably 
found  during  the  paroxysms 
of  the  disease  in  the  blood  of 
animals  which  have  acquired 
surra  either  naturally  or  ex- 
perimentally. Although  blood 
containing  these  infusoria 
readily  communicates  the  dis- 
ease to  susceptible  animals  it 
entirely  loses  its  virulence 
when  it  is  filtered  through 
porcelain,  so  as  to  free  it  from 
the  parasite.  The  disease  can 
be  transmitted  to  healthy,  sus- 
ceptible animals  even  of  differ- 
ent species,  with  the  unfiltered  blood  of  a  diseased  animal. 
The  microscope  reveals  the  infusoria  in  vast  numbers  moving 
with  great  activity  in  the  blood.  When  this  acute  stage  has 
passed  the  organisms  disappear  ;  the  temperature  falls  ;  the 
severity  of  the  symptoms  abates  ;  and  there  is  an  intermission, 
during  which,  at  the  beginning  of  the  attack,  the  patient  may 
appear  in  good  health.  Although  the  blood  during  an  inter- 
mission may  appear  under  the  microscope  to  be  absolutely  free 
from  the  parasites,  its  inoculation  into  susceptible  animals  will, 
as  a  rule,  produce  the  disease.  The  blood  of  surra  affected 
horses  loses  its  power  of  transmitting  the  disease  by  inocula- 
tion in  about  eighteen  hours  after  death. 

Under  the  microscope,  these  parasites  are  detected  in  a  drop 
of  blood  by  an  irregularly  intermittent  and  characteristic  quiver- 
ing of  some  of  the  red  blood   corpuscles,  which  become  much 


Fig.  67.     Trypanosoma  Evansi, 
highly  magnified.   {After  Evans). 


ETIOLOGY  267 

altered  in  form.  The  leucocytes  remain  unchanged  in  appear- 
ance. After  a  further  and  careful  examination  of  this  slightly 
quivering  blood  a  minute  thread-like  organism  with  eel-like 
movements,  emerges  from  the  niass  of  corpuscles.  It  may  be 
seen  apparently  tugging  with  all  its  might  at  a  red  corpuscle 
endeavoring  to  detach  it  from  its  rouleau.  The  question  of  the 
manner  in  which  these  parasites  interfere  with  the  health  of 
the  affected  animal  has  not  yet  been  settled.  When  they  are 
outside  the  animal  body  and  in  a  dry  state,  they  are  killed  or 
rendered  inert  by  prolonged  atmospheric  heat. 


Fig.  68.     Photograph   of  blood  of  horse  containing   Trypanosoma . 
(  Taken  by  Smith  and  Kinyoun.  ) 

The  contagium  of  surra  is  fixed  and  can  be  conve3-ed  only 
by  inoculation  or  ingestion.  Stagnant  water  and  grass  growing 
on  recently  inundated  land  form  favorable  resting  places  for 
this  organism.  It  is  probable  that  flies  act  as  carriers  of  surra 
from  infected  animals  to  sound  ones,  especially  if  the  latter 
have  open  wounds. 

§200.  Symptoms.  The  symptoms  as  given  by  lyingard 
are    as    follows.      "The    chief    symptoms,   in  addition  to    the 


^68  SURRA 

ever,  are  the  occasional  appearance  of  an  urticarial  erup- 
tion, general  or  localized,  closely  following  the  first  rise  of 
temperature,  but  which  may  make  its  appearance  at  any  time 
during  the  course  of  the  disease  ;  then  the  presence  of 
petechiae  on  the  mucous  membranes,  chiefly  that  covering  the 
membrana  nictitans,  lachrymation  and  the  exudation  of  a 
semi-gelatinous  material  into  the  subcutaneous  and  other  con- 
nective tissues.  There  is  rapid  wasting  and  great  weakness, 
although  in  the  majority  of  cases  the  appetite  remains  good 
throughout,  no  matter  how  high  the  fever.  There  is  extreme 
pallor  of  the  visible  mucous  membranes,  and  this  is  followed  at 
a  later  period  by  yellowness.  From  first  to  last  there  is  pro- 
gressive anaemia  ;  the  blood  at  first  presents  a  normal  char- 
acter, but  after  a  varying  period  of  time  it  undergoes  marked 
changes.  The  white  corpuscles  are  increased  in  number  and 
the  red  corpuscles  usually  cease  to  form  normal  rouleaux,  lose 
their  individuality  and  run  together  forming  irregular  masses. 
They  are  at  first  dark,  but  gradually,  as  the  disease  advances, 
almost  entirely  lose  their  coloring  matter  and  become  pale.'' 

The  respective  duration  of  the  paroxysms  and  intermissions 
is  very  irregular.  Lingaid  puts  it  down  as  from  one  to  six 
days.  He  states  that  in  a  few  experimental  horses  the 
paroxysms  lasted  from  eighteen  to  twenty-two  days. 

The  period  of  incubation  seems  to  be  liable  to  great  varia- 
tions. It  may  be  put  from  six  to  eight  days  after  inoculation 
or  ingestion  of  blood  taken  from  an  animal  suffering  from 
surra.  It  appears  from  Lingard's  investigation  that  the  period, 
of  latency  may  be  prolonged  to  thirteen  days,  if  the  blood  used 
for  inoculation  has  been  taken  from'  a  dead  animal.  \\'hen  the 
parasites  have  been  given  in  water,  by  the  mouth,  symptoms 
of  surra  may  not  appear  for  even  seventy-five  days.  We  have 
no  exact  data  for  determining  the  time  required  for  the  disease 
to  become  manifest  under  natural  conditions  from  drinking 
surra  contaminated  water.  Gunn  states  that  the  average  dura- 
tion of  the  disease  is  about  fifty-two  days. 

§  20I.  Morbid  anatomy.  As  a  rule  there  is  great 
•emaciation,  enlargement  of  the  liver  and  spleen,  petechiae  on 
various  internal  organs,  and  a  yellow^  or  amber  colored  jelly- 


MORBID    ANATOMY  269 

like  exudation  in  the  connective  tissue  of  the  throat,  chest 
and  abdomen,  about  the  muscles  and  other  tissues,  and 
especially  round  the  base  of  tlie  heart.  The  lungs  often  show 
sio;ns  of  inflammation.  The  mucous  membranes  and  other 
tissues  are  frequently  tinged  yellow  by  the  coloring  matter  of 
the  bile. 

Steel  noticed  ulceration  of  the  stomach  in  about  two-thirds 
of  his  cases  among  mules  in  Burma.  In  India  this  ulceration 
has  not  been  observed  among  horses  as  a  sequence  of  surra. 

The  clinical  aspect  of  surra  is  essentially  one  of  progres- 
sive anaemia,  accompanied  by  paroxysms  and  intermissions, 
during  both  of  which  there  is  a  gradual  decrease  in  the  num- 
ber of  the  red  blood  corpuscles  and  in  the  amount  of  hemo- 
globin in  the  blood,  with  consequent  anaemia  of  the  visible 
mucous  membranes. 

The  importance  of  this  disease  renders  it  desirable  to 
reprint  "A  preliminary  note  on  a  parasitic  disease  of  horses," 
by  Capt.  Allen  M.  Smith  and  Dr.  J.  J.  Kinyoun  from  the 
Army  Pathological  Laboratory,  Manila,  Oct.  17,  1901,  as  it 
gives  a  good  idea  of  the  appearance  of  the  disease.  The 
accompanying  photograph  showing  trypanosoma  was  taken 
by  Smith  and  Kinyoun  at  that  time. 

"On  October  15,  1901,  information  was  given  us  by  J.  W.  Jobling, 
Assistant  Bacteriologist  of  the  Board  of  Health  of  Manila,  that  an  epi- 
demic sickness  of  an  undetermined  nature  was  now  prevailing  in  this 
city,  and  also  that  he  had  just  taken  a  specimen  of  blood  from  a  sick 
animal  which  on  examination  revealed  the  presence  of  a  parasite, 
whether  this  was  accidental  or  was  the  causative  agent  of  the  disease  in 
question,  he  was  unable  to  say.  On  investigation  and  enquiry  it  was 
learned  from  the  Veterinarian  in  charge  of  the  corral  of  the  Quarter- 
masters Department,  and  from  the  City  Veterinarian,  that  there  was  now, 
and  had  been,  a  fatal  epidemic  among  the  horses  in  Manila,  the  Quarter- 
masters Department  having  lost  over  200  within  the  past  four  months. 

One  of  the  corrals  was  visited  by  us  on  the  15th  inst.,  where  we  were 
shown,  by  the  Veterinarian  in  charge,  20  horses  and  mules,  ill  with  an 
undetermined  disease.  These  animals  presented  the  several  stages  of 
the  malady,  some  were  quite  recently  attacked,  while  others  had  been  ill 
for  over  two  months. 

The  symptoms  first  noticed  are  :  impairment  of  appetite,  constipa- 
tion, fever  and'  thirst.  These  are  followed  within  a  few  days  by  a  rapid 
and  progressive  emaciation. 


270  SURRA 

The  temperature  for  the  first  few  days  ranges  from  104°  to  loj'^  F., 
the  pulse  is  full  and  strong.  This  may  be  termed  the  acute  stage.  Then 
begins  an  asthenic  state,  which  may  terminate  fatally  within  a  variable 
period,  or  by  a  slow  convalescence.  During  this  stage,  usually  within  lo 
daj's  after  the  onset,  there  appears  a  commencing  oedema  above  the 
belly,  involving  the  soft  parts,  coincident  with  this,  or  soon  after,  the 
tedema  extends  to  the  feet  and  legs.  The  pulse  becomes  rapid,  weak 
and  dichrotic,  the  respiration  increased,  shallow  and  jerky,  the  gait 
staggering.     Emaciation  is  rapid  and  extreme. 

The  disease  has  a  tendency  to  relapse,  this  may  occur  at  any  time, 
even  after  convalescence  appears  to  have  been  fully  established.  The 
relapses  are  invariably  fatal. 

The  mortality  in  this  epidemic  has  been  about  75  per  cent  for  Ameri- 
can horses  and  mules,  and  100  per  cent  for  native  ponies. 

The  gross  pathology  shows  serous  effusions  into  the  pleurae,  peri- 
cardium, and  sometimes  the  peritoneum.  There  is  also  a  serous  exudate 
into  the  cellular  tissue  of  the  legs  and  abdomen.  The  organs  are  pale, 
but  otherwise  normal  in  appearance. 

At  the  time  of  our  inspection,  five  acute  cases  w-ere  examined,  the 
duration  of  the  attack  being  from  six  days  to  two  weeks.  All  these 
animals  presented  the  several  clinical  appearances  as  above  described. 

Blood  specimens  were  taken  from  the  jugular  vein  of  each  and 
examined  microscopically,  shortly  afterwards.  In  4  of  these  a  parasite 
was  demonstrable.  The  other  was  negative,  but  a  specimen  taken  the 
following  day  showed  the  presence  of  this  same  parasite. 

On  the  day  following,  specimens  were  obtained  from  12  others,  all 
chronic  cases,  with  the  result  of  finding  this  same  parasite  in  the  blood 
of  four.  In  three  they  were  very  few,  whilst  in  the  fourth,  the}-  were 
present  in  great  numbers,  as  many  as  20  could  be  seen  in  one  microscope 
field.  The  animal  from  which  the  specimen  was  taken  had  suffered  a 
relapse. 

It  would  appear  that  the  parasite  may  disappear  from  the  peripheral 
circulation,  or  exists  there  in  such  few  numbers  that  it  is  not  easily 
demonstrable,  after  the  acute  stage  has  passed,  it  would  require  repeated 
blood  examinations  to  decide  this  point. 

Description  of  the  parasite.  The  parasite  resembles  a  whiplike 
worm,  having  much  the  appearance  of  the  Trichocephalus  Dispar,  its 
length  is  from  10  to  14  mikrons,  and  is  from  i.  to  1.2  mikrons  in  diameter 
through  its  body,  the  neck  is  nearly  h  its  length,  tapering  graduall}-  to 
a  point  representing  the  mouth  (?).  It  has  a  limiting  membrane,  which 
is  well  defined,  the  contour  is  in  most  cases,  symmetrical,  but  in  some 
the  body  line  is  quite  irregular.  The  larger  part  of  the  parasite  (body) 
contains  granular  material  and  clear  spaces,  which  latter  vary  in  size  and 
number;  they  are  irregularly  distributed,  and  may  encroach  on  the  wall 
so  as  to  cause  irregular  outline.  The  granular  material  does  not  extend 
to  the  neck. 


SMITH    AND    KINYOUN's    DESCRIPTION  27! 

The  parasite  is  actively  motile,  having  both  a  vermicular,  (con- 
tractile) and  spiral  movement.  It  moves  forward  in  a  very  peculiar 
manner,  the  long  whiplike  process  is  thrust  forward  by  a  spirillar 
motion,  followed  by  a  contracture  of  the  body. 

We  have  not  so  far  been  able  to  determine  its  intimate  structure, 
further  than  the  limiting  membrane,  and  the  protoplasmic  substance  of 
the  body. 

Two  sizes  of  the  parasite  have  been  seen  in  all  the  specimens  exam- 
ined, the  larger  appears  to  be  more  numerous,  and  contains  considerably 
more  granular  material  than  the  smaller,  and  usually  two  or  more 
vacuoles.  Whether  these  two  sizes  represent  male  and  female,  has  not 
been  determined.  We  are  inclined  to  believe  from  our  observations, 
that  these  do  represent  the  male  and  female,  because  we  have  observed 
in  more  than  half  the  fresh  specimens,  the  joining  of  a  large  and  small 
parasite  in  such  a  way  as  to  appear  to  be  something  more  than  accidental. 

The  pathological  changes  caused  by  this  parasite  is  a  rapid  distruc- 
tion  of  the  red  blood  cells,  causing  an  acute  anaemia.  The  changes 
occur  in  the  blood  coincident  to  the  invasion  of  the  parasite.  In  one 
horse  which  had  been  ill  seven  days,  the  red  blood  cells  numbered 
3,500,900,  the  white,  14,500.  In  another,  ill  six  weeks,  the  red  blood 
cells  were  3,200,000,  and  the  white  were  13,900.  The  blood  of  a  healthy 
horse,  taken  as  a  comparison,  gave  red  blood  cells,  6,900,000,  white, 
9,800.  There  is  also  a  slight  diminution  in  the  amount  of  htemaglobin, 
about  85  per  cent. 

After  convalescence  has  been  fully  established,  no  parasite  can  be 
found,  the  blood  gradually  assumes  its  normal  constitution. 

The  parasite  is  not  confined  to  the  blood,  as  it  can  be  demonstrated 
in  the  serous  effusions. 

It  is  quite  easy  to  detect,  all  that  is  necessary  is  to  make  a  micro- 
scopical examination  of  fresh  blood  films,  a  i  in.  objective  will  suffice. 
Dried  films,  fixed  and  stained  with  any  of  the  nuclear  dj'es. 

The  organism  appears  to  be  a  strict  parasite.  It  lives  but  a  short 
time  after  removal  from  the  body,  the  longest  time  which  it  has  been 
kept  alive  in  blood  serum,  was  not  more  than  ten  hours. 

The  parasite  has  many  of  the  properties  in  common  with  the  filaria, 
and  resembles  more  nearh'  that  of  filaria  perstans,  only  it  is  smaller, 
and  its  movements  dissimilar.  Yet  on  the  other  hand,  the  clinical  his- 
tory of  animals  infested  by  it,  the  changes  occurring  in  the  blood,  the 
lesions  observed  in  post  mortem,  point  very  strongly  towards  its  classifi- 
cation with  the  spirochaete. 

The  mode  of  transmission  has  not  yet  been  studied.  It  does  not 
appear  to  be  highly  contagious,  as  it  does  not  appear  to  spread  from  one 
to  another,  even  under  the  most  favorable  circumstances. 

It  more  nearly  resembles  malaria  in  this  respect.  It  is  more  than 
probable  that  its  extra  corporeal  state  is  different,  or  another  supposition 


272  SURRA 

equally  tenable,  is  that  its  intermediate  host  is  some  insect,  such  as  the 
fl\'  or  mosquito."' 

§  202.  Differential  diagnosis.  Surra  is  to  be  differen- 
tiated from  anthrax.  A  history  of  the  case  or  outbreak  to- 
gether with  the  chronic  course  and  intermittent  temperature 
in  surra  will  usually  suffice  to  determine  the  nature  of  the  dis- 
ease. If  no  history  or  symptoms  are  known,  the  diagnosis 
can  be  made  post-mortem  from  the  bacteriological  examination 
of  the  tissues  or  blood  as  Bad.  anthracis  is  readily  found  in 
cases  of  anthrax. 

§203.  Prevention.  Lingard  has  demonstrated  quite  con- 
clusively that  one  attack  does  not  prevent  a  horse  from  a  sub- 
sequent one.  The  experience  in  the  surra  infected  districts 
shows  that  the  best  way  to  prevent  the  occurrence  of  this  dis- 
ease among  horses  is  ( i)  to  see  that  their  water  supply  is  pure  ; 
(2)  to  avoid  giving  them  grass  or  hay  taken  from  marshy 
or  inundated  ground  ;  and  (3)  to  exclude  the  excrements  of 
rats  from  the  grain.  Lingard  found  that  arsenic  has  a  decided 
effect  in  diminishing  the  number  of  surra  organisms  in  the 
blood  of  affected  animals. 

§  204.  Trypanosomiasis.  Stiles  has  introduced  this 
term  to  describe  an  infection  with  parasites  belonging  to  the 
flagellate  family  Trypanosomidae .  The  term  is  analogous  to 
Taeniasis  or  Coccidiosis .  There  are  a  number  of  different  kinds 
of  trypanosomiasis  now  recognized  and  considered  by  certain 
writers  to  be  very  closely  related  being  caused  by  species  of 
parasites  belonging  to  the  same  genus.  Among  these  Stiles 
has  mentioned  the  following,  viz.  : 

1.  Surra.  A  disease  of  equines,  camels,  elephants  and 
certain  other  animals  in  India,  attributed  to  Trypanosoma 
JEvansi. 

2.  Nagana,  nygana  or  Tsetse-fly  disease  of  Africa. 
Affecting  cattle,  horses,  mules,  asses,  antelopes,  camels  and 
certain  other  animals.      It  is  attributed  to  Typanosoma  Brucci. 

3.  Doiirine  or  maladie  du  edit  of  Algiers,  France  and 
Spain.  It  attacks  the  horse  and  the  assin  particular,  but  may 
be  transmitted  to  certain  other  animals  ;  it  is  attributed  to 
Trypanoso7na  equiperdum. 


TRYPANOSOMIASIS  273 

4.  Mai  dc  caderas  of  South  Africa.  It  affects  horses, 
asses,  cattle,  hogs  and  certain  other  animals,  and  is  attributed 
to  Tjypanosoma  equiman. 

5.  Rat  fn'Pa?iosomiasis  SLttrihnted  to  Trypanosoma  Lezvisi. 
By  some  authors  this  parasite  is  alleged  to  be  identical  with 
the  horse  surra  organism,  but  it  is  quite  certain  that  rats  may 
harbor  a  distinct  species. 

Until  the  results  of  further  investigations  are  recorded  it 
is  deemed  best  to  consider  these  as  distinct  infections. 

REFERENCES. 

1.  Burke.  Surra  or  progressive  pernicious  anaemia.  Vet.  Jour., 
London  Vol.  XXV.     1887. 

2.  Burke.  Surra,  pernicious  anaemia  in  the  lower  animals.  Vet. 
Jour.,  London.     Vol.  XXVI.     p.  309. 

3.  Burke.  Microorganisms  and  disease,  especialh-  with  reference 
to  the  question.   What  is  the  pathology  of   "  surra  "  in  animals?      Vet. 

Jour,  and  Ann.  Coinp.  Patli.  London.     Vol.  XXVIII.   (1889).   p.  25. 

4.  Durham.    Tsetse  disease.      Veterinarian.     Vol.  LXXI.     (  1S98). 

5.  Evans.  Report  on  surra  disease  in  the  Dera  Ismail  Khan  District. 
1880.      Military  Department. 

6.  Evans.  On  a  horse  disease  in  India  known  as  "surra," 
probably  due  to  a  Hsematozoon.  Vet.  Jour.,  London.  Vol.  XIII. 
(iSSi).  'July,  Aug.,  Sept.,  Nov. 

7.  HassaIvI^.  Bibliography  of  surra  and  allied  Trypanosomatic 
diseases.    Butt.  No,  42,  U.  S.  Bureau  oj  Animal  Industry.    1892.     p.  132. 

8.  Kanthack.  On  nagana  or  tsetse  fly  disease.  Report  made  to 
the  tsetse  fly  committee  of  the  Royal  society,  etc.  Proc.  Royal  Soc, 
Lotidon.     Vol.  LIV. 

9.  Lingard.     Report  on  horse  surra.      1S93.      (Bombay.) 

10.  Lingard.  Report  on  "  surra  "  in  equines,  bovines,  buffaloes 
and  canines,  etc.     Ree.  de  med.  vet.     Par.  8.     Vol.  VIII.     p.  377. 

11.  Noc.\RD.  vSur  les  rapports  qui  existent  entre  la  dourine  et  le 
surra  ou  le  nagana.      Coinp.  rend.  Soc.  de  biol .     Vol.  LIU.      (1901). 

12.  Ranking.  A  preliminary  note  on  the  nature  and  pathology  of 
the  disease  known  as  "surra"  affecting   horses    and    mules   in    India. 

Vet.  Jour.,  London.     Vol.  XXXII.     (1891). 

13.  Salmon  and  Stiles.  Emergency  report  on  surra.  Bulletin 
No.  42,  U.  S.  Bureau  of  Annual  Industry.     1S92. 

14.  Steel.  On  relapsing  fever  of  equines.  Vet.  Jour.,  London. 
Vol.  XXII.      (1886). 

15.  Steel.  Report  upon  an  obscure  and  fatal  disease  among 
transport  mules  in  British  Burma.      1885. 

16.  Smith  .\nd  Kinvoun.  A  preliminary  note  on  a  parasitic  dis- 
ease of  horses.     Army  Pathological  Laboratory,  Manila.    Oct.  17,  1901. 

17.  Stiles.  Trypanosoma  in  a  new  role.  Am.  Med.  Vol.  III.  ( 1902). 


274  INFECTIOUS    DISEASES 

DOURIXE. 

Synonyms.  Venerial  disease  of  solipeds  ;  equine  syphilis  ; 
maladie  du  coit  ;  chancerous  epizootic  ;  breeding  paralysis  : 
epizootic  paraplegia. 

§  205.      Characterization.      A    contagions   affection    of 
solipeds,  transmitted   by  copulation  and  attended  by   specific 
lesions  of  the  generative  organs  and  nervous  sj^stem,  such  as 
local   venereal    swellings,    chancerous    ulcers   and    cicatrices, 
dementia  and  paralysis. 

The  disease  is  essentially  an  equine  one,  although  the 
following  specie^  are  susceptible  to  experimental  inoculation, 
namely  ;  dogs,  rabbits,  rats,  mice  and  asses.  While  the  horse 
shows  the  greatest  susceptibilit}-,  the  ass  is  comparativeh- 
resistant  to  the  infection. 

§  206.  History.  Dourine  has  existed  for  a  long  time. 
It  was  first  clearh'  described  in  1796  by  Amnion  who  found  it 
in  the  royal  stud  at  Trakchnen  in  Northern  Prussia.  We 
have  later,  1801  and  1807  descriptions  of  the  disease  in  the 
same  localit3\  It  was  found  in  Bromberg  in  18 17  to  1820,  in 
Austria  and  Bohemia  in  1S21-8,  in  Syria  in  1821,  in  Switzer- 
land in  1830,  in  France  in  1830-32,  in  Siberia  in  1833-40,  in 
Italy  in  1836,  in  Russia  in  1843,  in  Poland  in  1830-40,  in 
Algiers  in  1847-55.  In  Syria  and  Asia  generally  it  is  reported 
to  appear  perennialh-. 

It  is  not  known  to  have  invaded  Belgium,  Scandinavia, 
England,  South  America  or  Australia.  All  indications  point 
to  Asia  and  Northern  Africa  as  the  home  of  the  disease  where 
it  still  appears  perennially. 

It  was  found  in  Bloomington,  111.,  in  1882.  The  first 
animal  showing  the  disease  was  a  brown  stallion  that  had  been 
imported  from  France.  In  this  locality  it  spread  to  a  consid- 
erable number  of  breeding  mares  and  stallions.  The  disease 
was  very  largely  stamped  out  of  that  region  by  a  rigid  quaran- 
tine of  diseased  and  exposed  animals.  Some  exposed  animals 
had,  however,  left  the  district,  and  it  is  not  surprising  that 
isolated  centers  of  infection  are  occasionally  found. 

§  207.  Etiology.  Thanhoffer  found  in  the  blood,  vaginal 
mucus,  testicle,  semen,   spinal  fluid   and   roots   of    the   dorsal 


ETIOLOGY  275 

and  lumbar  nerves  bacteria,  especially  streptococci  and  less 
constantly  bacilli,  to  which  he  attributed  the  cause.  More  re- 
cently Schneider  and  Buffard  have  apparently  demonstrated  that 
a  protozoon,  one  of  the  Trypanosomae ,  is  the  specific  pathogenic 

agent. 

The  Trypanosoma  varies  greatly  in  form  at  different  stages 
of  its  growth.  In  the  exudate  of  the  ear  tumefaction,  without 
as  yet  other  symptoms,  it  is  found  as  minute  granules  in  groups 
or  larger  spherical  bodies  resembling  very  large  micrococci, 
each  having  a  nucleus.  There  are  larger  bodies  in  which  a 
delicate  membranous  covering  encloses  one,  two  or  three  masses 
of  chromatin  which  extend  to  form  one  or  more  points  (club 
shaped  or  fusiform).  Each  chromatin  mass  has  a  nucleolus 
on  its  outer  surface  or  slightly  apart  from  it.  Twenty-four 
hours  later  there  may  be  added,  (i)  short,  thick  chromatin 
bodies  with  two  slightly  undulating,  pointed,  membranous  pro- 
longations ;  (2)  more  delicate,  fusiform  bodies,  each  with  one 
chromatin  nucleus,  a  detached  nucleolus,  and  the  membrane 
prolonged  into  two  actively  moving  flagella  ;  (3)  larger  pyri- 
form  bodies  with  chromatin  nuclei  and  nucleoli  and  the  mem- 
brane prolonged  into  one  or  several  flagella  ;  (4)  fusiform 
hodies  thick  or  delicate,  each  having  a  chromatin  nucleus  and 
nucleolus,  and  arranged  singly  or  in  groups  of  two,  four,  six 
or  more  united  together  at  one  end  and  diverging  at  the  other. 
These  last  are  20  to  30yu  long  by  1.5  to  2//  broad  and  perhaps 
may  be  the  adult  form  of  the  parasite  from  which  the  small 
granular  or  spore  forms  found  in  the  most  recent  lesions  are 
derived.  The  fusiform  outline,  the  deep  staining  central  mass 
with  its  adjacent  nucleolus,  and  the  pointed  or  flagellated  mem- 
branous prolongations,  more  or  less  motile  or  undulating  are 
characteristic  features. 

In  its  morphology  and  evolutionary  forms  the  trypanosoma 
of  dourine  has  not  been  shown  to  differ  from  that  of  surra. 
The  granule  form,  the  spherical,  the  club  shaped  or  pyriform 
bodies,  the  fusiform  with  more  or  less  stellate  groupings  seem 
to  be  generic  characteristics.  The  specific  distinction  is  found 
in  the  pathogenesis  as  shown  by  the  two  diseases  (surra  and 
dourine). 


276  DOURINE 

In  the  active  cutaneous  or  mucous  lesions  the  parasite  is 
usually  found  abundantly  in  the  blood,  semen,  milk,  vaginal 
secretions  and  the  erosions  of  the  vaginal  mucosa  and  penis. 
During  intermissions,  however,  and  in  the  absence  of  local 
lesions,  the  parasites  are  not  found  in  the  blood  on  microscopic 
examination,  yet  the  inoculation  of  the  blood  into  a  dog  will 
usually  produce  the  disease.  The  parasite  disappears  from 
the  blood  and  tissues  very  rapidly  after  death,  so  that,  to  prove 
successful,  inoculations  should  be  made  from  an  infected  indi- 
vidual before  or  immediately  after  death.  They  are  not  effec- 
tive after  forty-eight  hours. 

Schneider  and  Buffard,  Nocard  and  others  found  the  try- 
panosoma  in  the  blood  and  exudates  of  horses,  asses  and  dogs, 
suffering  from  dourine.  They  failed  to  find  it  in  the  same 
localities  in  animals  of  the  same  species  which  were  free  from 
dourine.  The  infected  blood  preserved  for  24  hours  in  sealed 
glass  tubes,  and  then  inoculated  into  dogs  produced  character- 
istic symptoms  and  lesions  with  the  many  trypanosoma  in  the 
blood.  Inoculation  into  two  other  dogs,  with  the  same 
material,  but  at  the  end  of  48  hours,  produced  a  slight 
transient  hyperemia  only,  without  local  lesions  or  propagation 
of  the  parasite  in  the  blood.  The  blood  from  the  same  animal 
inoculated  after  fifteen  da^-s  gave  negative  results. 

§  208.  Symptoms.  The  first  local  changes  in  the  genital 
organs  begin  after  a  period  of  incubation,  according  to 
Maresch,  of  from  eight  days  to  two  months.  The  first  symp- 
tom in  the  stallion  consists  in  the  swelling  of  the  glans  penis. 
Reddish  spots,  vesicles  and  ulcers  may  occur  on  the  outer  sur- 
face of  the  penis.  The  meatus  urinarius  is  reddened  and 
swollen  and  exhibits  a  mucous  discharge.  The  animal  has  a 
continuous  desire  to  micturate  and  frequently  manifests  sexual 
excitement.  The  swelling  also  spreads  from  the  penis  to  the 
sheath  and  scrotum  in  which  case  the  testicles  become  in- 
flamed. Finally,  ,  the  inguinal  glands  and  lymph  vessels 
become  involved.  These  local  affections  may,  as  the  disease 
advances,  almost  entirely  dissappear.  In  some  cases  the  ex- 
ternal changes    are    absent,  as  the  mucous  membrane  of   the 


SYMPTOMS  277 

urethra    is    first    affected  ;    the  only    visible    symptoms   beiug 
strangury  and  a  mucous  discharge  from  the  urethra. 

In  mares,  the  disease  begins  with  a  doughy  or  tense  swell- 
ing of  the  pudenda,  which  frequently  spreads  to  the  udder  and 
inner  surface  of  the  thighs.  The  mucous  membrane  of  the 
vagina  is  red  in  spots  and  swollen,  sometimes  thickened  by 
g-elatinous  elevations  and  covered  with  a  turbid  and  orange 
colored  secretion.  Sometimes  nodules,  vesicles  and  ulcers  are 
observed  on  the  mucous  membrane.  They  are,  however,  fre- 
quently absent.  In  mares,  the  local  manifestations  are  often 
insignificant.  The  mucous  membrane  in  the  neighborhood  of 
the  clitoris  is  more  congested  than  at  other  parts  and  the  cli- 
toris itself  is  swollen  and  erect.  At  the  same  time  affected 
mares  show  excessive  sexual  excitement.  They  frequently 
suffer  from  strangury  and  after  considerable  straining  urine  is 
discharged  in  small  jets. 

Instead  of  urine  small  quantities  of  sticky,  discolored 
mucus  are  discharged.  The  animals  incessantly  shake  their 
tails  and  open  and  close  the  vagina  in  rapid  succession,  showing 
the  clitoris  as  mares  do  in  season.  The  discharge  often  exerts 
a  corrosive  action  on  the  tail  and  legs.  In  severe  cases  the 
neighboring  lymph  glands  become  inflamed  and  swollen  as 
well  as  the  udder,  on  which  abscesses  may  appear.  The  swell- 
ing may  even  extend  to  the  hypogastrium. 

The  general  symptoms  develop  only  after  weeks  or  even 
months  ;  their  appearance  is  often  delayed  until  the  local 
symptoms  have  disappeared.  At  first  the  animals  are  depressed 
and  weak,  they  frequently  continue  to  lift  up  their  hind  feet, 
alternately,  so  as  to  try  to  avoid  putting  weight  upon  them, 
knuckle  on  their  fetlock  joints  and  lose  control  over  the  move- 
ments of  their  hind  legs  while  walking. 

It  is  reported  that  stallions  especially  suffer  from  an 
uticaria  in  the  form  of  sharply- defined,  round,  flat  eminences 
which  may  be  raised  the  breadth  of  a  finger  above  the  surface 
and  which  may  vary  in  size  from  two  to  four  centimeters  or 
more  in  diameter.  These  eminences  are  caused  by  a  serous 
infiltration  of  the  papillary  layer  of  the  skin  in  the  neighbor- 
hood of  a  small  artery  and  are  evidently  of  a  vaso-neurotic 


278  DOURINE 

character.  The}-  often  appear  and  disappear  very  rapidly  and 
may  shift  their  position.  Usually  they  persist  for  several 
weeks  during  which  time  they  become  moderately  hard  and 
then  slowly  disappear.  Their  favorite  sites  are  the  croup, 
neck,  shoulders,  chest  and  abdomen. 

Later  in  the  course  of  the  disease,  a  progressive  paralysis 
of  the  hind  quarters  combines  with  excessive  emaciation.  The 
animal  has  a  staggering  gait  and  often  gives  wa}-  on  the 
pasterns  and  at  the  knees,  can  rai.se  itself  from  the  ground 
onl}^  with  difficulty — and  .sometimes  falls  down  unexpectedly. 
The  affected  stallion  is  unable  to  cover,  as  he  can  neither 
mount  a  mare  nor  get  an  erection.  Some  patients  exhibit 
permanent  tremblings  over  the  whole  body  or  local  paralysis 
as  for  instance,  that  of  the  lips,  ears  and  eyelids.  Hyperaes- 
thesia  of  the  skin  is  observed  particularly  in  stallions  and 
with  it  is  extensive  pruritis,  so  that  the  animal  continually 
rubs  itself,  bites  the  affected  parts  and  thus  produces  extensive 
sores  on  the  skin.  The  patient  becomes  extremely  emaciated 
especially  in  the  hind  quarters  so  that  the  outlines  of  the  pelvic 
bones  and  ribs  become  ver}' prominent.  The  skin  becomes  drj-, 
the  hair  is  ruffled  and  loses  its  gloss.  Some  animals  manifest 
pain  when  the  lumbar  region  is  pressed.  The  senses  become 
more  and  more  blunted  and  the  eyes  assume  a  staring  and 
expressionless  appearance.  As  the  end  approaches  the  patient 
persistently  maintains  a  recumbent  position  and  finall)-  dies 
from  the  effect  of  secondary'  lesions  such  as  hypostatic  inflam- 
mation of  the  lungs,  septicaemia  or  perhaps  general  cachexia. 
Sometimes  in  the  final  stage  the  patient  suffers  from  nasal 
catarrah  with  swelling  of  the  submaxillar}'  glands  and  con- 
junctivitis. Severe  internal  inflammation  of  the  eyes  has  been 
observed.  The  appetite  continues  longer  than  any  of  the 
other  normal  functions. 

§  209.  Morbid  anatomy.  In  the  early  .stages  there  are 
phlegmonous  or  oedematous  swellings  of  the  sheath,  scrotum, 
penis  and  inguinal  glands  and  a  yellowish  liquid  effusion  into 
the  scrotal  cavit}-.  The  skin  covering  the  parts  may  show  a 
papular  or  vesicular  eruption  or  if  this  has  passed  a  mottling 
with  white  spots  shows  where  these  lesions  have  been.      Later, 


MORBID    ANATOMY  279 

the  inguinal  glands  shrink  and  become  firm  owing  to  the  de- 
velopment of  fibroid  tissue.  The  testicles  which  are  either 
swollen  or  shrunken,  contain  foci  of  suppuration  or  caseation. 
The  connective  tissue  of  the  epididymis  and  the  cord  is  the  seat 
of  a  gelatinous  exudate.  The  walls  of  the  scrotum  may  be 
greatly  thickened  and  the  seat  of  abscesses  or  of  caseous  degen- 
erations. Iij  advanced  cases  the  testicles  are  usually  abnor- 
mally small  even  if  the  scrotal  mass  is  enormously  distended. 
The  .sheath  and  penis  may  be  the  seat  of  more  or  less  numerous 
ulcers  and  swellings.  Contraction  and  contortions  of  the  penis 
are  not  uncommon.  It  may,  however,  retain  its  normal  dimen- 
sions. The  walls  of  the  lymphatics  in  the  inguinal  region 
may  be  the  seat  of  hyperplasia,  the  thickening  causes  them  to 
stand  out  like  cords  as  in  glanders,  in  the  advanced  stages 
the  muscles,  especially  those  of  the  hind  limbs,  become  pale 
and  atrophied.  The  nerve  centers  undergo  profound  changes 
which  have  been  studied  by  Thanhoffer.  The  pia  mater  in 
the  affected  part  of  the  spinal  cord  is  the  seat  of  active  conges- 
tion and  thickening.  The  central  canal  of  the  cord  is  dilated 
more  at  one  point  than  another,  contains  more  than  the  nor- 
mal amount  of  liquid  and  the  neuroglia  around  it  is  thickened 
and  fibrous.  The  substances  of  the  cord,  both  white  and  gray, 
show  congestion,  blood  staining,  at  points  foci  of  softening  and 
at  others  induration  (hyperplasia  of  the  neuroglia).  The  nerve 
cells  are  modified  in  various  ways,  some  being  granular,  some 
discolored  by  fine  granular  pigment,  some  having  enlarged 
and  multiplied  nuclei  and  some  show  vacuoles.  The  nerve 
filaments  often  show  a  granular  degeneration  extending  from 
the  nerve  cell  to  the  axis  cylinder.  The  latter  is  liable  to  be 
varicosed  or  enormously  enlarged.  In  the  affected  portion  of 
the  cord  leucocytes  are  numerous  and  there  is  often  hyper- 
plasia. The  neuroglia  tend  to  increase  and  apart  from  the  foci 
of  softening  tend  to  give  a  special  firmness  to  the  substance. 
The  subarachnoid  and  subdural  fluid  is  increased  and  there  may 
be  at  the  roots  of  the  spinal  nerves,  especially  in  the  dorsal 
and  lumbar  regions,  a  gelatinoid  exudate  investing  the  nerve, 
distending  the  connective  tissue  beneath  the  neurilemma  and 
even    occupying    the    interval    between    the    nerve  filaments. 


28o  DOURINE 

Sometimes  large  corpuscular  bodies    are   found   between    the 
nerve  fibers. 

The  cerebral  meninges  are  congested  and  opaque.  Foci 
of  softening  are  by  no  means  uncommon  and  the  cerebral 
ventricles  contain  an  abnormal  quantity'  of  fluid. 

The  bou}'  tissue  generally  has  lost  its  consistency  and  the 
medullary  matter  may  be  unduly  reddened.  The  large  joints 
contain  an  excess  of  synovia  of  a  somewhat  pinkish  color.  The 
ligaments  of  the  hip  joint  are  often  congested,  thickened  and 
softened.  The  articular  cartilages  may  even  show  areas  of  blood 
staining. 

The  intestines  are  usually  nearly  empty,  soft,  pale  and 
flaccid.  Ruthe  has  in  one  case  observed  rounded  ulcers  on  the 
mucosa. 

The  mesentery  is  thickened  with  an  infiltration  and  it  has 
a  yellowish  discoloration  and  the  mesenteric  glands  are  usually 
enlarged,  softened  and  friable  though  sometimes  firm  and  con- 
tracted. The  lymph  glands  adjoining  the  generative  organs 
are  often  swollen,  pigmented  and  studded  with  foci  of  casea- 
tion, varying  in  size  from  that  of  a  pea  upward.  The  liver  is 
softened,  hyperemic  or  fatty.  The  spleen  is  small.  The  kid- 
neys are  usually  large,  pale  and  blackened.  The  thoracic 
organs  may  show  little  change,  though  hypostatic  congestions 
and  foci  of  caseation  or  suppuration  may  be  present.  The 
blood  is  light  colored  and  forms  a  loose,  pale  clot.  There  is  a 
diminution  in  the  number  of  red  blood  cells  and  a  relatively 
large  increase  in  the  number  of  leucocytes. 

In  the  mare,  in  addition  to  the  lesions  in  the  internal  organs 
and  blood,  the  following  may  be  noted  in  connection  with  the 
generative  system.  Phlegmons  or  oedematous  swellings,  or 
ulcers  on  the  lips  of  the  vulva  and  on  the  vulvar  and  vaginal 
mucosae.  The  parts  become  variously  distorted.  A  crop  of 
pustules  or  vesicles,  which  run  into  ulcers  may  appear  on  the 
urethral  orifice,  the  vulva  and  adjacent  skin.  The  mammary 
glands  are  sometimes  inflamed,  oedematous  and  tender,  with 
suppurative  or  necrotic  foci.  The  adjacent  lymph  glands  are 
enlarged  by  infiltration  or  contracted  by  sclerosis 


PREVENTION  281 

In  the  dog  the  symptoms  and  the  lesions  resemble  those  in 
the  horse. 

§  210.  Prevention.  The  prevention  of  this  disease 
seems  to  rest  in  the  isolation  of  all  affected  animals.  It  is 
important,  therefore,  that  its  diagnosis  be  made  at  the  earliest 
possible  moment. 

REFERENCES. 

1.  BUFFARD  AND  Schneider.  Prophylaxie  de  la  dourine  et  expose 
de  faits  nouveaux  interessant  cette  nialadie.  Jour,  de  Med.  Vet.  et  de 
Zoolch.     1 90 1. 

2.  FAViLtE.  Extirpation  of  nialadie  dii  coit.  Annual  Report, 
Bureau  of  Animal  Industry.     1S95-6,  p.  13  and  62. 

3.  Thanhoffer.     tiber  Ziichilahme.    Wien.     1S8S. 

4.  Wilson-Barker.  Maladie  du  coit  in  Nebraska.  Vet.  J.  Land. 
Vol.  XXXV.     (1892).     Vol.  XXXVI.     {1893). 


CHAPTER    VH. 


INFECTIOUS   DISEASES    FOR    WHICH    THE    SPECIFIC 
CAUSE  IS  NOT  YET  DETERMINED. 


RINDERPEST. 


Synonyms.  Contagious  typhus  ;  steppe  murrain  ;  cattle 
plague. 

§  211.  Characterization.  Rinderpest  is  the  most  fatal 
disease  affecting  cattle.  It  is  a  specific  eruptive  fever  occur- 
ing  both  sporadically  and  in  epizootics.  It  is  characterized  b}- 
a  more  or  less  typhoid  condition,  with  lesions  largel}'  located 
in  the  mucosa  of  the  digestive  tract  and  skin  and  by  the  infec- 
tious nature  of  all  of  the  tissues,  secreta  and  excreta.  It  is 
a  disease  peculiar  to  cattle,  although  other  ruminants  are 
susceptible  to  it. 

§212.  History.  Rinderpest  seems  to  have  been  brought 
to  western  Europe  by  the  importation  of  cattle  from  central 
Asia  as  early  as  the  fourth  century.  It  is  supposed  that  it 
had  long  existed  on  the  steppes  of  central  Asia  and  eastern 
Europe.  The  first  great  epizootic  of  which  there  seems  to  be 
records  occurred  about  1709  and  spread  over  nearlj^  all  of  the 
countries  of  Europe.  It  is  reported  that  1,500,000  cattle  died 
from  its  effects  during  the  years  from  171 1  to  1714.  Ramaz- 
zini  seems  to  have  been  the  first  (1711)  to  accurately  describe 
the  symptoms  and  lesions. 

It  was  in  connection  with  this  disease  that  the  first  veteri- 
nary police  regulations  were  instituted  and  it  is  stated  that 
because  of  the  ravages  of  this  affection  that  Veterinary  Col- 
leges were  first  established  with  Government  aid.  In  the  latter 
half  of  the  eighteenth  century  rinderpest  was  prevalent  in 
nearly  all  of  the  countries  of  Europe.     During  the  years  1740 


RINDERPEST  283 

to  1750  it  was  estimated  that  three  million  cattle  died.  The 
importance  of  this  disease  is  shown  in  the  fact  that  in  Italy 
alone  during  the  year  1792  from  three  to  four  million  of  cattle 
died  from  its  effects.  In  the  years  1844  to  1845,  Russia  is  said 
to  have  lost  a  million  of  cattle  from  this  disease  alone.  Nearly 
all  of  the  countries  of  Europe  have  from  time  to  time  lost 
heavily  from  it.  It  is  stated,  however,  that  England  and 
Germany  have  .practically  freed  themselves  from  it.  Preven- 
tive inoculation  against  this  disease  was  introduced  into  Eng- 
land by  Dodson  as  early  as  1744  and  later,  by  Courtivron,  into 
France. 

§  213.  Geographical  distribution.  Rinderpest  is  a 
well  known  cattle  plague  in  Russia  and  the  steppes  of  central 
Asia.  It  has  extended  from  time  to  time  from  its  home  in 
Rus.sia  and  Asia,  to  nearly  every  country  in  Continental 
Europe  and  Asia.  More  recently  it  has  occured  in  southern 
Africa  and  the  Philippines.  It  has  not  been  introduced  into 
the  United  States  or  other  American  countries.  At  present, 
it  is  not  known  to  exist  in  England,  although  in  the  past  she 
has  suffered  many  destructive  epizootics. 

§  214.  Etiology.  The  specific  etiological  factor  of  rin- 
derpest is  not  known.  Several  investigators  have  isolated  and 
studied  various  species  of  bacteria  from  the  tissues  of  animals 
dead  from  this  disease.  Semmer  of  Dorpat  has  always  found 
the  same  organism  in  the  lesions.  His  results  do  not  appear 
to  have  been  verified.  There  seems  to  be  no  doubt  in  the 
minds  of  those  who  have  worked  on  this  disease  that  it  is 
caused  by  a  specific  microorganism,  most  likely  a  species  of 
bacteria.  Koch  makes  the  following  statement  concerning  the 
etiology  of  rinderpest  in  the  second  report  of  his  investigations 
in  South  Africa  in  1897.  "^^^  efforts  to  find  by  means  of  the 
microscope,  as  well  as  through  cultivation,  a  specific  micro- 
organism in  the  blood  have  as  yet  been  fruitless.  I  also  did 
not  succeed  in  finding  any  specific  microorganisms  amongst  the 
microbes  which  the  mucus  from  the  nose,  the  secretions  from 
mucous  membranes,  and  the  contents  of  the  intestines  naturally 
contain  in  large  numbers." 

The  virus  may  be  transmitted  from  the  sick  to  the  healthy 


284  RINDERPEST 

individuals  in  a  variety  of  vt-ays.  both  direct  and  indirect.  It 
is  said  to  be  present  in  the  various  excreta  of  the  diseased 
animal,  such  as  the  discharges  from  the  nose,  the  saliva,  the 
urine  and  the  feces.  It  retains  its  vitality  outside  of  the  body 
in  a  moist  state  for  months,  even  a  year  or  more,  according  to 
some  authorities.  Hence  feces  and  the  fodder  and  bedding 
soiled  by  the  discharges  may  convey  the  disease.  When  dried, 
however,  its  vitality  is  .said  to  be  lost  in  a  iew  days.  Persons 
may  carry  the  virus  on  their  shoes,  clothing  and  farm  imple- 
ments. Even  small  animals,  such  as  cats  and  rats,  which  fre- 
quent barns  and  stables  have  been  looked  upon  as  carriers  of 
the  infection. 

It  is  also  claimed  that  animals  after  having  passed  through 
one  attack  of  the  disease  are  able  to  resist  successfully  future 
attacks.  Inoculation  with  the  virus  is  said  to  produce  im- 
munity, but  the  process  of  inoculation  itself  is  followed  by 
death  in  many  cases.  The  disease  is  reported  to  have  devel- 
oped after  feeding  hay  a  year  after  it  has  lain  in  an  infected 
stable.  It  is  destroyed  at  a  temperature  of  131°  F.  but  in 
animal  tissues  it  re.sists  putrefaction. 

§  215.  Symptoms.  The  symptoms  of  rinderpest  are 
those  of  a  severe,  acute,  infective  disease.  The  period  of  in- 
cubation is  stated  to  be  from  six  to  nine  days.  At  first  the  tem- 
perature rises  to  105  to  106°  F.  and  remains  near  that  point  with 
but  slight  variations  until  other  symptoms  develop.  The  pulse 
is  small,  beating  from  60  to  120  per  minute.  There  is  great 
debility,  decrease  in  the  yield  of  milk  and  loss  of  appetite  : 
rumination  becomes  disturbed  and  the  animal  may  have  slight 
attacks  of  shivering. 

After  these  preliminary  symptoms  there  are  well  marked 
rigors,  respiration  becomes  accelerated  and  the  visible  mucous 
membranes  assume  a  scarlet  color.  There  is  entire  loss  of 
appetite,  arrest  of  the  function  of  rumination,  thirst,  consti- 
pation with  the  feces  dry  and  covered  with  mucus.  Some- 
times there  is  slight  colic.  Later  there  is  a  discharge  which 
is  first  serous  and  subsequently  sero-raucous  from  the  eyes, 
nose  and  vagina.  The  saliva  flows  from  the  mouth.  The 
feces  gradually  become  thinner  until  violent  diarrhoea  accom- 


MORBID    ANATOMY  285 

panied  by  colic  sets  in.  The  evacuations  become  foetid,  viscid 
and  sometimes  mixed  with  blood.  The  animal  becomes  rapidly 
emaciated,  staggers  when  walking,  is  very  sensitive  to  pressure 
on  the  loins  and  lies  down  a  great  deal.  In  exceptional  cases 
the  patient  manifests  nervous  symptoms.  Others  exhibit  violent 
dyspnea  and  symptoms  of  severe  inflammation   of  the  lungs. 

As  the  disease  advances  characteristic  changes  are  to  be 
seen  in  the  mucous  membranes.  Red  patches  which  may  be 
flat  or  in  the  form  of  wheals  and  which  quickly  become  covered 
with  a  greyish  white,  loose  crust  appear  on  the  mucous  mem- 
brane of  the  lips,  tongue,  cheeks,  gums,  nostrils  and  vagina. 
The  uppermost  epithelial  layer  consequently  becomes  opaque 
and  yellowish  gray  spots  develop  on  it.  Less  frequently  crusts 
are  formed  from  the  tumors  by  their  caseous  disintegration. 
The  crusts  on  being  shed,  leave  dark  red  hollow  places,  the 
so  called  erosion  ulcers,  which  readily  bleed.  In  slight  cases 
of  the  disease  there  may  be  no  crusts  or  erosions.  It  is  stated 
that  sometimes  an  eruption  in  the  form  of  very  minute  pimples 
and  pustules  occurs  on  the  abdomen,  inner  surface  of  the 
thighs,  perineum  and  udder.  In  these  cases  it  may  be  con- 
fused with  that  of  variola.     Pregnant  animals  frequently  abort. 

In  sheep  and  goats  the  disease  is  milder,  and  its  infectious- 
ness is  said  to  be  less  than  in  cattle,  although  the  symptoms 
are  essentially  the  same.  Sheep  are  reported  to  suffer  fre- 
quently from  pneumonic  affections  when  attacked  by  rinder- 
pest. 

§  216,  Morbid  anatomy.  Authors  differ  somewhat  on 
the  lesions  characteristic  of  this  disease.  Walley  has  pointed 
out  the  fact  that  none  of  the  morbid  changes  are  constant  and 
consequently  they  vary  with  the  stages  of  the  epizootic,  the 
condition  of  the  animal  and  the  treatment.  There  is  always 
emaciation,  the  muscular  tissue  is  dark  and  capillary  conges- 
tion is  marked.  All  the  tissues  of  the  body  may  be  the  seat 
of  effusions,  exudations  and  blood  extravasations.  If  symp- 
toms referable  to  the  nervous  system  have  occurred,  brain 
lesions  will  be  found  at  post  mortem. 

The  muscle  of  the  heart  is  pale,  relaxed  and  blood  extra- 
vasations beneath  the  endocardium  are  not  rare.     The  kidneys 


286  RINDERPEST 

are  usualh'  the  seat  of  congestion  or  ecchymoses  either  beneath 
the  capsule  or  in  their  structure.  There  are  also  parenchyma- 
tous changes.  The  liver  may  be  pale,  congested,  engorged 
with  blood  or  ecchymotic  beneath  the  capsule.  The  bile  is 
thin.  There  are  more  or  less  parenchymatous  changes  in  the 
liver  cells.  The  lymphatic  glands  generally  are  usually 
enlarged  and  the  mesenteric  glands  are  often  hyperemic  or 
even  hemorrhagic. 

The  structures  most  often  affected  are  the  mucous  mem- 
branes of  the  digestive,  respiratory  and  genito-urinary  tracts 
and  the  skin. 

Nodules  and  pustules  are  sometimes  found  on  the  skin, 
especially  on  the  udder.  The  mucous  membrane  of  the  mouth 
and  pharynx  is  congested  in  spots,  swollen  and  exhibits 
rounded,  yellowish  grey,  caseous  plates  or  deposits.  The 
removal  of  the  plates  discloses  ulcerous  and  highly  congested 
depressions  in  the  mucous  membrane,  the  so  called  erosion 
ulcers.  These  changes  are  best  marked  on  the  inner  surface 
of  the  lips,  lower  surface  of  the  tongue,  buccal  mucous  mem- 
brane and  gums  of  the  inferior  maxilla. 

In  the  first  three  stomachs  the  mucous  membrane  is 
usually  congested  in  spots  and  the  epithelium  is  so  loose  that 
it  can  be  easily  detached.  The  contents  of  the  rumen  and 
reticulum  are  soft  and  those  of  the  omasum  are  often  dried,  a 
condition  that  is  met  with  in  many  other  diseases.  In  some 
cases  the  contents  of  the  omasum  are  fluid.  Generally  the 
abomasum  is  empty,  and  contains  only  a  small  quantity  of 
tough,  muco-purulent,  yellow  or  sanious  material.  Its  mucous 
membrane  is  highly  congested,  especially  in  the  neighborhood 
of  the  pyloric  orifice.  The  congestion  is  partly  diffuse,  parth^ 
in  spots,  in  the  form  of  points  or  streaks.  Its  color  may  be 
purple  or  reddish-brown  with  a  tinge  of  slate-grey.  The 
epithelium  exfoliates.  On  the  mucous  membrane  may  be 
found  small,  brownish-yellow,  caesous  deposits,  in  the  form  of 
plates,  which  become  detached  in  shreds,  leaving  indented, 
highly  reddened  areas  which  are  studded  with  petechiae.  The 
glands  (peptic  and  mucous  glands)  of  the  stomach  are  swollen 
and  show  considerable  cellular  hypertrophy.     Like  changes 


DIFFERENTIAL    DIAGNOSIS  287 

are  present  in  the  small  intestine,  where  there  is  a  good  deal 
of  swelling  and  congestion  of  the  mucous  membrane  with 
insulated,  scab-like  caseous  deposits  and  erosions.  In  very 
severe  cases  these  deposits  form  tube-like  casts  of  the  intestinal 
canal.  At  the  same  time  there  may  be  considerable  infiltration 
of  the  solitary  glands  and  of  Peyer's  patches  which  are  swollen 
and  either  undergoing  a  purulent  disintegration  or  becoming 
covered  with  caseous  or  purulent  deposits. 

In  the  large  intestine  the  inflammatory  changes  are  much 
less  pronounced.     They  are  greatest  in  the  caecum. 

The  nasal  mucous  membrane  is  of  a  dark  red  color  and 
covered  with  greyish-yellow,  soft  scabs.  After  they  are  re- 
moved, the  true  tissue  of  the  mucous  membrane  lies  bare. 
Similar  changes  are  found  in  the  larynx  and  trachea,  where 
the  deposited  masses  are  frequently  purulent  and  of  a  creamy 
con.sistence.  The  lungs  are  sometimes  hyperaemic,  sometimes 
oedematous,  hepatised  or  emphysematous.  Pneumothorax 
and  subcutaneous  emphysema  may  be  present. 

§  217,  Differential  diagnosis.  It  is  very  difficult  to 
diagnose  rinderpest  from  the  first  cases  that  occur  especially  if 
there  is  no  history  of  infection.  The  diagnosis  is  based  upon, 
the  symptoms,  morbid  anatomy,  progress  of  the  epizootic  and 
the  history.  The  most  characteristic  diagnostic  symptoms  are 
the  rise  in  temperature  (which  often  occurs  some  days  before 
other  symptoms),  formation  of  red  spots  and  a  yellow  coating 
on  the  visible  mucous  membranes  and  later  the  development  of 
erosion  ulcers.  A  mucous  discharge  from  the  mouth,  nares, 
eyes  and  vagina  with  symptoms  of  severe  intestinal  disturbances 
and  excessive  emaciation  are  of  differential  value. 

Rinderpest  is  to  be  differentiated  from  "  foot  and  mouth  " 
disease  in  which  the  foot  lesions  are  absent  or  where  it  is  com- 
plicated with  fever.  Malignant  catarrah  if  complicated  with 
emphysema  of  the  lungs.  Anthrax,  Texas  fever,  and  other 
affections  such  as  contagious  pleuropneumonia  and  enteritis 
may  be  mistaken  for  it.  The  differentiation  must  be  made 
from  the  specific  nature  of  each  disease. 

§  218.  Prevention.  In  this  connection  the  proclama- 
tion for  the  prevention  of  the  spread  of  rinderpest  in  Cape 


288  RINDERPEST 

Colony  recently  issued  by  the  British  Government  authorities 
is  of  interest.      It  is  as  follows  : 

1.  '"Disinfection  of  hides,  hoofs,  horns,  skins  and  feathers,  i.  Hides, 
skins,  hoofs,  horns  and  feathers  will  only  be  allowed  south  of  Orange 
River  and  will  only  be  accepted  for  conveyance  by  rail  after  being 
thoroughly  disinfected  in  the  manner  hereafter  described  at  railway 
stations  and  the  authorized  crossing  places  in  terms  of  Regulation  5 
issued  under  Proclamation  No.  387  of  1896,  or  at  each  of  them  as  shall 
hereafter  be  notified. 

2.  No  hides,  skins,  horns  or  hoofs  shall  be  passed  by  the  Supervis- 
ing Officer  unle,ss  accompanied  by  a  declaration  signed  by  the  consignor 
(or  his  agent)  that  they  are  from  animals  that  have  not  died  from  rinder- 
pest. Any  hides,  skins,  horns  or  hoofs  not  accompanied  by  such 
declaration,  shall  be  immediaiely  destroyed  by  the  Supervising  Officer 
at  the  consignor's  expense. 

3.  Disinfection  shall  be  supervised  by  the  officer  appointed  by  the 
Government  for  the  purpose,  but  shall  be  performed  by  the  owners  or 
consignors  or  their  agents. 

4.  Dried  hides,  horns  or  hoofs  shall  be  immersed  in  a  liquid  disin- 
fectant for  at  least  30  minutes. 

5.  Green  hides  and  skins  shall  be  immersed  in  a  liquid  disinfectant 
for  a  period  of  at  least  15  minutes. 

6.  The  disinfectant  used  may  be  either  a  two  per  cent  solution  of 
carbolic  acid  or  a  five  per  cent  solution  of  Jaye's  Disinfectant,  Odam's 
Disinfectant  or  Izal. 

7.  Feathers  shall  be  hung  up  for  three  hours  in  a  chamber  charged 
with  sulphurous  acid  produced  by  burning  an  excess  of  sulphur  in  a 
closed  chamber. 

S.  Hides,  skins,  horns,  hoofs  and  the  packages  containing  feathers 
when  disinfected,  shall  be  marked  for  the  guidance  of  the  railway 
officials,  and  shall  be  accompanied  by  a  certificate  that  disinfection  has 
been  efficiently  performed,  signed  by  the  supervising  officer  without 
which  the  railway  officials  shall  refuse  to  receive  the  articles. 

9.  When  disinfection  is  completed,  the  articles  disinfected  shall  be 
loaded  direct  into  a  previously  disinfected  railway  truck. 

10.  Drying,  salting  or  any  other  subsequent  treatment  of  the  hides 
or  skins  shall  be  done  by  the  owners  or  their  agents  at  their  own  risk." 

''Disinfection  of  travelers  or  passengers,  i.  Travelers  and  pas- 
sengers shall  be  disinfected  at  railway  stations  and  at  authorized  cross- 
ing places,  in  terms  of  Regulations  7  and  8  issued  under  Proclamation 
No.  587  of  1896,  by  the  police  or  other  persons  duly  authorized  by  the 
Secretary  of  Agriculture  in  the  manner  hereafter  described. 

2.  Natives  shall  strip  and  enter  a  bath  containing  2  per  cent  solu- 
tion of   carbolic  acid  ;   they  shall  then  be  provided  with  a  blanket  or 


PREVENTION  289 

Other  suitable  clothing  until  the  clothes  they  are  wearing  have  been 
disinfected. 

3.  The  clothing  of  all  natives,  and  the  blankets,  rugs,  karrosses, 
wraps,  etc.,  of  all  Europeans,  whether  from  disinfected  areas  or  not, 
shall  be  subjected  to  sulphurous  acid  fumes  produced  by  burning  an 
excess  of  sulphur  in  a  closed  chamber  for  at  least  15  minutes,  pending 
arrival  and  erection  of  a  proper  steam  disinfecting  apparatus. 

4.  Europeans  coming  from  an  infected  farm  or  place  or  who  have 
otherwise  rendered  themselves  liable  to  infection  from  contact  with  na- 
tives or  their  huts  or  kraals,  shall  be  disinfected  in  such  manner  as,  in 
the  discretion  of  the  disinfecting  officer,  may  be  deemed  necessary  and 
their  clothing  as  provided  by  clause  3. 

5.  The  disinfectant  to  be  used  shall  be 

2  per  cent  solution  of  carbolic  acid  or 

5  per  cent  solution  of  Jaj^e's  Fluid  or 

5  per  cent  solution  of  Odam's  Disinfectant  or 

5  per  cent  solution  of  Izal. 

6.  Boots  of  Europeans  and  natives  shall  be  well  drv  brushed,  and 
then  the  uppers  and  soles  well  wiped  with  the  disinfecting  solution  by 
means  of  cloths. 

7.  Europeans  on  coming  from  an  infected  farm  or  place  and  all  na- 
tives on  presenting  themselves  at  a  railway  station,  siding,  halt  or  other 
place  north  of  the  Orange  River,  shall,  before  the  station  master,  clerk, 
guard  or  other  officer  permits  them  to  obtain  a  traveling  ticket,  hand  to 
the  station  master  or  booking  clerk  a  certificate  signed  by  the  disinfect- 
ing officer  in  terms  of  Form  A,  to  the  effect  that  they  and  their  clothes 
have  been  properly  disinfected  as  well  as  such  articles  and  things  in 
their  possession  as  are  intended  to  be  carried  by  rail,  not  being  articles 
or  things  actually  prohibited  to  be  carried  south  of  the  Orange  River. 

8.  Any  European  coming  from  an  infected  farm  or  place  or  who 
has  not  in  any  way  been  liable  to  infection,  shall  sign  a  certificate  to 
that  effect  in  terms  of  Form  B,  and  without  such  certificate  shall  be 
deemed  as  coming  from   an   infected   farm  or  place,  or  otherwise  been 

iable  to  infection,  and  shall  be  subject  to  all  provisions  and  regulations 
attached  to  persons  coming  from  infected  areas  or  liable  to  infection  ; 
and  if  the  above  certificate  contains  any  false  statement  the  person  sign- 
ing the  same  will  be  liable  to  a  penalty  not  exceeding  100  pounds  or,  in 
default  of  payment,  to  imprisonment  with  or  without  hard  labor,  for  a 
period  not  exceeding  six  months." 

Rinderpest. 

FORM   A. 

This  is  to  certify  that together  with  his 

clothes  and  the  articles  or  things  in  his  possession,  authorized  to  be  car- 
ried by  rail,  have  been  properly  disinfected  as  required  by  the  Government 
Regulations. 

Disinfecting  Officer. 


290  CONTAGIOUvS    PtEURO-PNEUMOXIA 

Rinderpest. 

FORM    B. 

I of do   hereby 

certify  that  I  have  not  come  from  any  farm  or  place  infected  with  rin- 
derpest, and  I  have  not  in  any  way,  to  the  best  of  my  knowledge  and  belief 
come  in  contact  with  infection. 

(Signed.) 

REFERENCES. 

1.  Danvsz,    Brodet   and   Theiler.       The    Vet.  Journal.      Vol. 
XLVI.     (1898).     p.  298. 

2.  Edington.     Report  of  Investigation.      The  Veterinary  Journal. 
Vol.  XLVI.     (1898).     p.  64. 

3.  Gamgee.     The  cattle  plague.     London.     1866. 

4.  Koch.     Report.     The  Veterinary  Journal.    XLV.  (1897)  p.  204. 

5.  Ram.JlZzini.     Dissertatio  de  Contagiosa  Epidemica,  Padua.  1711. 

6.  Turner  and  Kolle.     Report  of  investigations.    The  Vet.  Jo2ir. 
Vol.  XLV.     (1897.)     p.  462. 

7.  WallEY.     The  four  bovine  scourges.     London.     1879. 


CONTAGIOUS  PLEURO-PNEUMONIA  IN  CATTLE. 

Synonyms.     Lung  plagtie  ;  pleuro-pneumonia  zymotica. 

§219.  Characterization.  Contagious  pleuro-pneumonia 
of  cattle  is  a  specific  epizootic  disease  which  affects  bovine 
animals  and  from  which  other  species  are  exempt.  When  the 
disease  results  from  exposure  in  the  usual  manner,  it  is 
characterized  by  an  inflammation  of  the  lungs  and  pleurae, 
which  is  generally  extensive  and  which  has  a  tendency  to 
invade  portions  of  these  organs  not  primarily  affected  and  to 
cause  death  of  the  diseased  portion  of  the  lung.  In  German^', 
it  is  known  as  Lungenseuche.  In  France,  it  is  spoken  of  as  the 
peripneumonie  contagieuse. 

§  220,  History.  The  first  account  of  the  appearance  of 
contagious  pleuro-pneumonia  dates  from  the  end  of  the  seven- 
teenth centur}'.  It  is  stated  that  it  was  observed  in  Hesse  for 
the  first  time  in  1693,  and  that  its  earliest  appearance  as  an 
epizootic  was  in  17 13  and  17 14,  when  it  prevailed  chiefly  in 
Switzerland  and  the  neighboring  countries  of  Wiirtemberg, 
Baden  and  Alsace.  There  are  detailed  reports  on  its  occur- 
rence from  the  year  1743.     In  1773,  Haller  published  an  essay 


HISTORY  291 

on  this  disease,  which  was  raging  severely  at  that  time  and 
described  the  symptoms,  anatomical  characters  and  protective 
measures  laid  down  by  the  sanitary  police.  In  1735,  the 
•disease  appeared  in  England  and  in  1765  in  France.  From 
1790  it  spread  over  the  whole  of  Germany,  France  and  Italy. 
At  the  commencement  of  the  nineteenth  century  over  all 
the  countries  of  Western  Europe. 

This  contagion  is  said  to  have  been  carried  to  Ireland 
from  Holland  in  1S39.  The  disease  was  brought  to  the  United 
States  at  several  different  times.  Probably  its  first  introduc- 
tion was  in  a  diseased  cow  sold  in  Brooklyn,  N.  Y.  in  1S43.  It 
came  to  New  Jersey  by  importing  affected  animals  in  1847. 
Massachusetts  was  infected  in  the  same  way  in  1859. 

South  Africa  was  infected  by  a  bull  brought  from  Holland 
in  1S54  and  Australia  received  the  contagion  with  an  English 
cow  in  1858.  It  is  also  reported  as  existing  in  various  parts  of 
the  continent  of  Asia  but  the  time  of  its  first  appearance  and 
the  extent  of  its  distribution  are  very  uncertain. 

Some  countries  which  had  only  been  infected  for  a  short 
time,  such  as  Norway,  Sweden  and  Denmark  have  succeeded 
in  eradicating  the  disease  wdthout  much  difiiculty  by  slaught- 
ering all  affected  and  exposed  animals.  Other  countries  long 
infected  and  in  which  the  contagion  was  thoroughly  estab- 
lished, like  Australia,  South  Africa,  Italy,  France,  Belgium 
and  parts  of  Germany  have  labored  long,  in  some  cases  mak- 
ing no  progress  and  in  others  being  only  partially  successful. 
Holland  was  one  of  the  first  of  the  thoroughly  infected  coun- 
tries to  free  itself  from  the  contagion. 

In  the  United  States,  Massachusetts  eradicated  pleuro- 
pneumonia during  the  period  from  i860  to  1866.  New  York 
and  New  Jersey  made  an  attempt  to  eradicate  it  in  1879  but 
were  not  successful.  Late  in  1883  the  contagion  w^as  carried 
to  Ohio,  probably  by  Jersey  cattle  purchased  in  the  vicinity  of 
Baltimore,  Md.,  to  which  place  it  had  extended  previous  to 
1868.  From  the  herd  then  infected  it  was  spread  by  the  sale 
of  cattle  during  1884  to  a  limited  number  of  herds  in  Illinois, 
to  one  herd  in  Missouri  and  to  two  herds  in  Kentucky.  By 
cooperation  between  the  United  States  Department  of  Agricul- 


292  CONTAGIOUS    PLEURO-PNEUMONIA 

ture  and  the  authorities  of  the  affected  states,  it  was  found 
possible  to  prevent  its  further  spread  and  to  completely  eradi- 
cate it  after  a  few  months. 

In  1886,  pleuro-pneumonia  was  discovered  in  some  of  the 
large  distillery  stables  of  Chicago  and  among  cows  on  neigh- 
boring lots.  This  led  to  renewed  efforts  to  secure  the  com- 
plete extirpation  of  this  disease  from  the  country.  Congress, 
in  1887,  enlarged  the  appropriation  available  for  this  purpose 
and  gave  more  extended  authority.  During  the  same  year  the 
disease  was  stamped  out  of  Chicago  and  has  not  since 
appeared  in  any  district  west  of  the  Allegheny  Mountains. 

The  work  of  eradication  was  at  the  same  time  commenced 
in  all  of  the  infected  States.  Before  the  end  of  the  year  1889- 
Pennsylvania,  Delaware,  Maryland,  the  District  of  Columbia, 
and  Virginia  had  been  freed  from  the  disease.  More  difficul- 
ties, how^ever,  were  encountered  in  the  States  of  New  York 
and  New  Jersey  on  account  of  the  larger  territory  infected 
and  the  density  of  the  population.  The  long  struggle  was 
crowned  with  success,  however,  and  the  last  animal  in  which 
the  disease  appeared  in  the  State  of  New  York  was  slaugh- 
tered early  in  1891  and  the  last  one  affected  in  New  Jersey 
met  the  same  fate  early  in  the  spring  of  1892. 

On  the  26th  day  of  September,  1892,  the  following  procla- 
mation was  issued,  declaring  the  United  States  to  be  free  from 
this  disease. 

PROCLAMATION— ERADICATION  OF  PLEURO-PNEUMONIA. 

U.  S.  Department  of  Agriculture, 
Office  of  the  Secretary. 

to  all  whom  it  may  concern  : 

Notice  is  hereby  given  that  the  quarantines  heretofore  existing  in 
the  counties  of  Kings  and  Queens,  State  of  New  York,  and  the  counties 
of  Essex  and  Hudson,  State  of  New  Jersey,  for  the  suppression  of  con- 
tagious pleuro-pneumonia  among  cattle,  are  this  day  removed. 

The  removal  of  the  aforesaid  quarantines  completes  the  dissolving 
of  all  quarantines  established  by  this  Department  in  the  several  sections- 
of  the  United  States  for  the  suppression  of  the  above-named  disease. 


ETIOLOGY  293 

No  case  of  this  disease  has  occurred  in  the  state  of  Illinois  since 
December  29,  18S7,  a  period  of  more  than  four  years  and  eight  months. 

No  case  has  occurred  in  the  state  of  Pennsylvania  since  September 
29,  1888,  a  period  of  four  years  within  a  few  days. 

No  case  has  occurred  in  the  state  of  Maryland  since  September  18, 
1889,  a  period  of  three  years. 

No  case  has  occurred  in  the  state  of  New  York  since  April  30,  1891, 
a  period  of  more  than  one  year  and  four  months. 

No  case  has  occurred  in  the  state  of  New  Jersey  since  March  25,  1892, 
a  period  of  six  months,  and  no  case  has  occurred  in  any  other  portion  of 
the  United  States  within  the  past  five  years. 

I  do  therefore  hereby  officially  declare  that  the  United  States  is  free 
from  the  disease  known  as  contagious  pleuro-pneumonia. 

J.  M.  RUSK,  Secretary. 

Done  at  the  city  of  Washington,  D.  C,  this  26th  day  of  September, 
A.D.,  1892. 

The  time  required  for  its  eradication  was  only   abottt  five 
years  and  the  total  expenditure  was  but  a  little  in  excess  of 

$1,500,000. 

§221.    Etiology.  The  specific  cause  of  contagious  pleuro- 
pneumonia has  not  been   fully  de^monstrated.     The  infection 
may  be  introduced  either  by  diseased  cattle,  or,  less  commonly, 
by  bearers  such  as  cattle   dealers,  attendants,  utensils,  fodder, 
dogs,  etc.     The  sheds   in   cattle   markets   are  very  dangerous 
centers  for  the  dissemination  of  the  disease.     All  cattle  are  not 
equally  susceptible.      It  is   generally  supposed  that  about  one 
animal  in  four  is  immune     The  virus  is  spread  principally  by  the 
respired  air.      Infected   cattle  are  reported  to  be  able  to  trans- 
mit it   even  during  the  period  of  incubation,  before  the  symp- 
toms are  apparent.     The  disease  is  particulary  infectious  when 
it  is  at  its  height  and  the  animal  remains  capable  of  transmitting 
the  disease  for    eight  or  ten  weeks  or   even   longer,  after   the 
infection,  especially  when  necrotic  foci   remain   in   the  lungs. 
Walley  estimates    the    duration    of  infectiousness   in  cases  of 
encapsuled  necrotic  foci  to  be  as  long  as  fifteen  months.      It  is 
said,  but  the  evidence  is  not  given,  that  the  virus  may  be  con- 
veyed by  the  respired  air  for  as  great  a  distance  as  forty  yards 
or  more.      In  exceptional  cases,  the  contagium  is  transmitted 
from  the  pregnant  cow  to  the  fetus. 


294  CONTAGIOUvS    PLEURO-PNEUMONIA 

Pols  and  Nolen,  in  1886,  at  Amsterdam,  found  round  mi- 
crococci always  present  in  the  exuded  matter  of  the  lungs. 
These  micrococci  were  about  0.9//  in  diameter  and  occurred 
either  isolated  or  in  chains  up  to  six  in  number.  In  the  un- 
stained preparation,  the  cocci  were  surrounded  by  a  distinct 
envelope  which  could  be  stained  only  with  great  difficulty 
and  which  was  absent  from  cultivated  micrococci. 

Arloing  believed  that  he  had  found  the  exciting  cause  of 
the  disease  in  various  bacilli,  especially  in  one  in  which  he 
C2i\\s pneumo-bacilhis  liqtiefaciens  bovis,  which  forms  short,  non- 
motile  rods.  Arloing  believes  that  his  experiments  prove  that 
the  pneumo-bacillus  is  the  cause  of  pleuro-pneumonia. 

In  1898,  Nocard  and  Roux  succeeded  in  obtaining  a  very 
feeble  growth  of  an  exceedingly  minute  organism  in  bouillon 
containing  cow  or  rabbit  serum  in  proportion  of  one  part  serum 
to  25  parts  bouillon,  when  cultivated  in  collodion  sacs  within 
the  abdominal  cavity  of  rabbits.  With  these  cultures  the 
disease  was  produced  in  cattle. 

§  222.  Symptoms.  The  symptoms  are  such  as  would 
be  expected  with  inflammation  of  the  lungs  and  pleurae,  but 
they  vary  considerably  according  to  the  course  which  the 
disease  runs.  If  the  attack  is  an  acute  one,  as  is  frequently 
seen  in  hot  weather,  the  symptoms  appear  suddenly.  The 
breathing  becomes  rapid  and  difficult,  the  animal  grunts  or 
moans  with  each  expiration,  the  shoulders  stand  out  from  the 
chest,  the  head  is  extended  on  the  neck,  the  back  is  arched, 
the  temperature  ranges  from  104  to  107°  F.,  the  milk  secretion 
is  suspended,  loss  of  appetite,  rumination  is  stopped,  the 
animal  may  bloat  and  later  be  affected  with  a  severe  diarrhoea. 
Such  cases  are  generally  fatal  in  from  seven  to  twenty  days. 

Very  often  the  attack  comes  on  slowly  and  the  symptoms 
are  more  obscure.  In  the  mildest  cases  there  is  a  cough  for  a 
week  or  two  but  no  appreciable  loss  of  appetite  or  elevation 
of  temperature.  The  lungs  are  but  slightly  affected  and 
recovery  soon  follows  vSuch  animals  may  disseminate  the 
virus  for  a  long  time  without  being  suspected  and  for  that 
reason  are  the  most  dangerous  of  all. 


SYMPTOMS  ,  295 

A  more  severe  tj'pe  is  commonly  seen.  The  cough  is  fre- 
quent, more  or  less  painful,  the  back  somewhat  arched  and  the 
milk  secretion  diminished.  These  symptoms  increase,  the 
appetite  is  affected,  the  animal  loses  flesh,  the  breathing 
becomes  more  rapid,  the  cough  more  painful,  pressure  of  the 
fingers  between  the  ribs  produce  evidence  of  tenderness,  the 
hair  loses  its  glo.ss  and  stands  erect,  the  skin  becomes  adher- 
ent, the  temperature  rises  to  103  or  105°  F.  Animals  thus 
affected  may  continue  to  grow  worse  and  die  in  from  three  to 
eight  weeks  or  they  may  after  a  time  begin  to  improve  and 
make  an  apparent  recovery.  The  inflammation  of  the  lung 
does  not,  as  a  rule,  subside  and  the  organ  returns  to  its  normal 
condition  as  in  ordinary  pneumonia,  but  wnth  this  disease  the 
life  of  the  affected  portion  of  the  lung  is  destroyed,  the  tissue 
dies  and  a  fibrous  wall  is  formed  around  it  to  shut  it  away 
from  the  living  parts.  The  tissue,  thus  encysted,  gradually 
softens,  becomes  disintegrated  and  breaks  down  into  pus.  The 
recovery,  therefore,  is  only  partial. 

By  those  accustomed  to  examining  the  lungs  of  cattle, 
other  and  extremely  important  symptoms  maybe  detected  dur- 
ino- the  course  of  the  disease.  By  auscultation  an  area  of  a 
certain  extent  may  be  found  where  the  natural  breathing  sound 
is  diminished  or  entirely  lost.  This  represents  the  diseased 
portion  of  the  lung.  In  other  cases  a  loud  blowing  sound  may 
be  heard,  quite  different  from  any  sound  produced  when  the 
lung  is  in  a  healthy  condition.  In  some  cases  crepitation  is 
heard  near  the  border  line  of  the  diseased  area  and  friction 
sounds  produced  by  the  roughened  pleura  may  be  detected. 
By  percussion  an  area  of  dullness  may  be  discovered  corre- 
sponding to  the  portion  where  the  respiratory  murmur  has 
disappeared.  This  loss  of  respiration  detected  by  auscultation, 
and  the  dullness  brought  out  by  percussion  are  the  most 
important  evidences  of  an  area  of  inflamed  or  consolidated  lung. 

Seriously  affected  animals  remain  standing  if  they  have 
sufficient  strength,  but  those  which  lie  down  are  said  to  always 
lie  on  the  affected  side. 

The  proportion  of  animals  that  become  affected  after  being 
exposed  varies  according  to  the  virulence  of  the  outbreak,  the 


296  CONTAGIOUS    PLEURO-PNEUMONIA 

susceptibility  of  the  animals  and  the  length  of  time  during- 
which  exposure  is  continued.  Sometimes  not  over  15,  20  or 
30  per  cent  of  the  animals  exposed  will  contract  the  disease 
while  at  other  times,  80  or  go  per  cent  may  be  infected. 
The  proportion  of  cases  in  which  the  disease  proves  fatal  also 
varies  greatly — it  may  not  exceed  10  per  cent  and  it  ma}' 
reach  50  per  cent.  In  general  it  ma}'  be  said  that  about  40 
per  cent  of  the  exposed  animals  will  contract  the  disease  and 
about  one-half  of  these  cases  will  prove  fatal. 

§  223.  Morbid  anatomy.  Anatomically  contagious 
pleuro-pneumonia  is  characterized  by  a  progressive  interstitial 
pneumonia  with  secondary  hepatization  of  the  lungs  and  exu- 
dative pleuritis.  Usually  only  one  lung,  the  left  as  a  rule,  is 
infected.  The  anatomical  changes  vary  according  to  the 
duration  of  the  disease. 

The  otherwise  healthy  lung  .shows,  in  the  initial  stage, 
small,  circumscribed,  inflammatory  centers  from  the  size  of  a 
hazelnut  to  that  of  a  walnut.  The  interlobular  tissue  in  it 
is  hyperaemic,  permeated  by  single  hemorrhages  and  infiltrated 
with  serum.  The  reddened  lobules  of  the  lungs  are  surrounded 
by  bright  margins,  which  are  i  to  2  mm.  broad  and  which 
are  filled  with  a  serous  or  lymphatic  fluid.  When  the  deposits 
are  superficial,  the  pleurae  become  opaque  and  covered  with 
slight  clots. 

At  the  height  of  the  disease  there  is  a  lobular  pneumonia 
with  pleuritis  which  is  usually  spread  over  the  greater  part  of 
one  lobe  of  the  lung.  The  lung  is  considerably  enlarged,  of 
firm  consistence,  very  heavy  (weighing  up  to  one  hundred 
pounds),  sinks  in  water  and  does  not  crackle  when  cut. 
Its  section  appears  marbled,  in  consequence  of  the  interstitial 
connective  tissue  having  become  thickened  into  broad  lines 
which  vary  in  color  from  orange  to  dirty  white  and  which 
surround  the  darker  colored  lobules  of  the  lung.  The  larger 
lobules  have  a  thickness  of  from  .5  to  2  cm.;  and  the  smaller 
ones  of  from  .25  to  .50  cm.  The  color  of  the  enclosed  lobules 
of  the  lungs  depends  on  the  duration  of  the  process  and  varies 
from  brown-red  to  dirty  yellow.  The  recently  infected  lobules 
have  a  blood-red,  reddish-brown    or  dark  brown  color   (stage 


MORBID    ANATOMY  297 

of  red  hepatization).  The  color  of  the  older  ones  varies  from 
orange  to  3'ellow  (yellow  hepatization)  and  that  of  a  still 
older  date  is  gray  (gray  hepatization).  The  central  foci,  be- 
cause the}'  are  the  oldest,  are  nsualh'  in  the  stage  of  yellow 
or  gray  hepatization.  Some  of  the  inclosed  lobules  of  the 
lungs  are  normal  or  only  compressed,  while  others  are  merely 
h\'peraemic.  If  we  closely  examine  the  bright  interstitial 
lines,  we  find  that  they  consist  at  first  of  an  oedematous 
infiltration,  which,  later  on,  becomes  plastofibrinous,  gelat- 
inous, indurated  and  finally  tends  to  the  formation  of  ad- 
ventitious connective  tissue.  The  lymph-spaces  in  the  lines 
are  dilated  like  lacunae  and  filled  with  a  serous  or  fibrinous 
fluid.  In  robust  animals,  the  exudate  in  the  alveoli  is  firm  ; 
but  is  of  a  more  serous  character  in  animals  of  a  weak  consti- 
tution. In  the  former  case,  a  section  made  through  the  lung 
will  be  found  to  be  granular.  Besides  these  changes,  the 
other  lymph  vessels  of  the  lungs  are  dilated,  their  walls  are 
infiltrated  with  cells  and  their  lumen  is  in  a  state  of  throm- 
bosis. The  blood-vessels  frequently  show  thrombi  and  small 
hemorrhagic  infarcts.  The  contents  of  the  finer  bronchi  are 
often  infiltrated  with  numerous  white  corpuscles.  The  bron- 
chial glands  and  frequently  the  mediastinal  glands  are  in- 
flamed and  swollen. 

The  pleurae  are  covered  with  .soft,  membranous,  fibrinous 
masses,  which  are  sometimes  lump}-  or  crumbling  and  which 
can  easily  be  detached.  These  deposits  have  a  reticular  sur- 
face and  may  attain  a  thickness  of  2  cm.  If  we  remove  them, 
we  shall  find  the  pleural  vessels  highly  injected  containing 
ecchymoses  and  the  surface  of  the  pleurae  in  a  rough  and 
uneven  condition.  In  the  thoracic  cavity  we  find,  in  varying 
quantity,  a  generally  inodorous  fluid  exudate,  which  may  be 
clear  or  opaque  and  which  contains  flakes  or  lumpy  masses. 
Similar  fibrinous  masses  often  lie  on  the  outer  surface  of  the 
pericardium. 

After  the  disease  has  existed  for  some  time,  the  affected 
parts  of  the  lungs  undergo  induration,  cicatrization,  caseation, 
calcification,  necrosis  or  suppuration.  At  first  the  interstitial 
infiltration   becomes  dense,  solid   and    dry    and   changes  into 


298  CONTAGIOUS    PLEURO-PNEUMONIA 

iirm  connective  tissue  which  makes  a  crunching  noise  while 
it  is  being  cut  with  the  knife.  In  other  places  we  have 
fatty  degeneration,  caseation,  calcification  or  suppuration,  in 
in  which  the  enclosed  lobules  of  the  lungs,  in  consequence  of 
the  existing  suppuration  become  gangrenous,  form  sequestra 
surrounded  b}'  sequestral  cavities  which  have  smooth  walls. 
The  dead  portions  of  the  lungs  may  remain  unchanged  in  these 
cavities  for  a  long  time.  Frequenth^  they  become  softened  to 
the  consistency  of  a  greas}^  yeast-like  paste.  Sometimes,  when 
they  are  comparatively  small,  they  become  absorbed,  and  a  scar 
is  formed.  The  hepatized  lobules  of  the  lungs  rarely  regain 
their  normal  condition  after  the  absorption  of  the  exudate. 
More  frequently  they  atroph}'  or  collapse,  undergo  atelectasis, 
calcification  or  softening,  become  necrotic  or  suppurating  or 
form  cavities.  On  the  pleurae  we  find  thick  and  wart-like 
h3^pertrophies  of  connective  tissue,  which  frequentl)'  cause  the 
lungs  to  adhere  to  the  side  of  the  chest. 

The  changes  in  the  lungs  and  pleurae  are  the  most  import- 
ant general  changes  in  cases  of  pleuro-pneumonia.  It  is 
stated  that  we  may  sometimes  meet  with  an  interstitial  fibrin- 
ous exudate  in  the  liver  with  atrophy  of  the  liver  cells  ;  sero- 
fibrinous effusions  into  the  articulations,  tendon  sheaths,  sub- 
cutis,  dewlap  and  brisket  :  intestinal  catarrh  ;  areolation  of 
Peyer's  patches  and  ulcers  on  the  gastro-intestinal  mucous 
membrane. 

The  views  of  pathologists  differ  as  to  the  nature  of  the 
earliest  changes  in  contagious  pleuro-pneumonia  and  it  is  not 
within  the  scope  of  this  work  to  present  imperfectly  developed 
or  controverted  theories.  Without  entering  into  a  discussion 
of  the  various  views,  it  is  clear  that  there  is  an  inflammatory 
condition  of  the  connective  tissue  between  the  lobules,  result- 
ing in  the  exudation  of  coagulable  lymph.  This  inflammation 
is  equally  marked  around  the  blood  vessels  and  air  tubes.  It 
leads  to  inflammatory  changes  in  the  inner  wall  of  the  veins 
and  these  cause  a  deposition  of  thrombi  or  plugs  in  the  vessels, 
which  prevent  the  return  of  the  blood.  The  blood  pumped 
into  the  lung  tissue  leaves  the  meshwork  of  capillaries  around 
the  air  vesicles,  enters  the  latter  and  produces  the  firm  hepa- 


DIFFERENTIAL    DIAGNOSIS  299 

tized  condition  so  characteristic  of  this  disease.  It  will  be 
easily  understood  how  the  diflferent  shades  of  color  from  dark 
red  to  grayish  or  yellowish  red  are  produced  if  we  bear  in 
mind  that  the  veins  in  different  parts  of  the  lung  tissue  are 
plugged  at  different  times  and  that,  the  affected  regions  are 
in  different  stages  of  the  disease. 

One  of  the  most  conspicuous  features  in  a  microscopic 
section  from  a  lung  affected  with  acute  contagious  pleuro- 
pneumonia is  the  presence  of  intensely  stained  foci  and  lines. 
These  lines,  to  which  Prof.  Welch  seems  to  have  been  the  first 
to  call  attention  are  visible  to  the  naked  eye  and  when  viewed 
with  a  hand  lens  suggest  by  their  peculiar  curves  the  contour 
lines  on  a  map.  They  are  situated  at  the  margin  of  and 
within  the  inflamed  connective  tissue  which  surrounds  the 
large  vessels  and  separates  the  lobules  from  one  another. 
A  closer  examination  of  these  lines  indicates  that  they  coincide 
with  the  boundaries  of  the  lobules  and  of  the  individual  lymph 
spaces  of  the  interlobular  tissue.  Under  a  high  power  of  the 
microscope  they  are  resolved  into  dense  masses  of  leucocytes 
in  various  stages  of  degeneration.  These  dense  bands  are 
presumably  attracted  to  the  connective  tissue  boundary  of  the 
lobules  and  to  the  walls  of  lymph  spaces  within  the  connective 
tissue  by  the  unknown  cause  of  the  inflammation,  presumably 
the  cause  of  the  disease  itself.  The  space  between  the  lines 
is  filled  with  fibrin,  in  which  ver^^  few  leucocytes  are  found. 

§224.  Differential  diagnosis.  It  is  extremely  difficult 
to  form  an  exact  diagnosis  of  the  disease  during  its  develop- 
ment, because  the  symptoms  which  are  present  are  few  in 
number  and  by  no  means  characteristic.  The  slight  fever 
and  cough  are  the  only  symptoms  of  diagnostic  importance  in 
the  prodromal  stage.  In  the  second  or  acute  stage  a  positive 
diagnosis  intt-a  vitam  can  be  made  only  when  cases  of  pleuro- 
pneumonia have  previously  occurred  or  when  several  occur 
simultaneously.  As  a -rule,  a  correct  diagnosis  can  only  be 
made  by  a  post  mortem  examination.  The  following  diseases 
are  to  be  differentiated  from  it  : — 

I.  Non-infectious  iiijiammation  of  the  lungs.  This  may  be 
distinguished  clinically,  as  a  rule,  by  its  more  acute  and  more 


300  CONTAGIOUS    PI.EURO-PNEUMONIA 

typical  course  and  by  its  sporadic  and  sudden  appearance 
and,  anatomically,  by  the  fact  that  the  parts  which  have 
undergone  hepatization  are  practically  all  of  the  same  age  and 
by  the  interstitial  lung  tissue  and  pleurae  being  but  slightly 
involved.  Nocard  states  that  in  exceptional  cases  pleuro- 
pneumonia may  run  a  very  acute  course  and  show  hepatiza- 
tion of  equal  ages. 

2.  Tuberculosis.  This  disease  cannot  be  positively  distin- 
guished clinically  from  pleuro-pneumonia.  Tuberculin  may  be 
used  as  a  diagnostic  agent,  although  it  is  not  at  all  certain 
that  animals  which  have  suffered  for  son:e  time  from  pleuro- 
pneumonia do  not  react  to  tuberculin.  After  all,  an  anatomi- 
cal examination  is  the  only  real  test.  Tuberculosis  and  con- 
tagious pleuro-pneumonia  have  occasionally  appeared  simul- 
taneously in  the  same  animal.  See  description  of  lesions  in 
tuberculosis. 

3.  Traumatic  pneumonia  or  pneumonia  due  to  foreign 
bodies  may  exhibit  the  .same  .symptoms  as  pleuro-pneumonia. 
Evidence,  during  life,  of  changes  in  the  heart  caused  by  trau- 
matic carditis  will  be  conclusive  in  making  the  differentiation. 

4.  Broncho  or  interstitial pneumojiia .      In  making  a  diag- 
nosis between  contagious  pleuro-pneumonia,  ba.sed  on  the  lung 
lesions  alone,  it  should  always  be  borne  in  mind  that  the  entire 
lungs  should  be  subjected  to  examination.     Attention  should 
be  given  to  signs  indicating  injury  to  the  chest  wall,  to  the 
possible  presence  of  foreign  bodies  and  to  severe  inflammation 
of  the  air  passages  which  may  result  from  the  aspiration  of 
irritant   or   corrosive   fluids.       Where   these    agents   may   be 
excluded  special  attention  should  be  paid  to  the  condition  of 
the  pleura  and  to  the  distribution  of  the  disease,  careful  notes 
being  made  of  the  lobes  involved.      Next  in  order  come  the 
peculiar    perivascular    and    interlobular   thickening    and    the 
thrombosis  of  the  veins.     Care  should  be  taken  not  to  con- 
found  mere  clots  with    adhesive   thrombi.      In   acute  pleuro- 
pneumonia,   after    death,   the    arteries  are   usually    distended 
with    clots.       The    different    features    of    the   hepatized    and 
oedematous  portions  of  the  lung   tissue  should    be  carefully 
noted.     Lastly,  the  peculiar  exudation  and  infiltration  in  the 


PREVENTION  301 


■connective  and  fatty  tissue  of  the  dorsal  mediastinum  and  of 
the  embedded  glands  should  not  be  overlooked.  With  the 
microscope  the  peculiar  dense  cell  masses  of  the  diseased  con- 
nective tissue  should  be  looked  for  and  the  nature  of  necrotic 
tissue  determined  in  case  microscopic  appearances  are  no 
longer  reliable  owing  to  hardening  processes. 

Finallj^  it  should  be  borne  in  mind  that  the  lesions  of 
broncho-pneumonia  and  the  interlobular  changes  which  may 
follow  it  may  coexist  with  contagious  pleuro-pneumonia,  and 
that  both  kinds  of  lesions  may  be  encountered  in  the  same 
lungs.  Hence,  great  caution  must  be  excercised  in  expressing 
an  opinion  when  only  a  small  portion  of  the  lungs  are  pre- 
sented for  examination,  because  only  that  portion  which  is 
affected  with  broncho-pneumonia  may  have  been  submitted. 

§  225.  Preventive  inoculation  and  eradication.  In 
Europe  inoculation  has  been  practiced  for  a  long  time  as  the 
principal  means  for  combatting  pleuro-pneumonia.  As  early 
as  the  beginning  of  the  last  century  it  was  proposed  in  Ger- 
many by  Hausmann  and  others.  Its  employment  was  greatly 
increased  by  the  investigations  which  were  made  in  1850  by 
Willems  in  Holland,  which  were  published  in  1852.  Since 
that  time  these  inoculations  have  been  practiced  in  nearly 
every  country.  The  literature  on  the  subject  is  very  copious. 
However,  the  value  of  inoculation  as  a  protection  against 
pleuro-pneumonia  has  not  yet  received  a  final  answer. 

The  advocates  of  inoculation,  among  whom  we  may  mention 
Haubner,  Bouley,  Schiitz  and  others  start  from  the  well  known 
fact  that  one  attack  of  pleuro-pneumonia  successfully  passed 
through,  confers  immunity  for  the  remainder  of  the  animal's 
life.  By  inoculation,  a  local,  specific,  inflammatory  process 
which  is  analogous  to  that  in  the  lungs,  is  produced  and  is 
followed  by  subsequent  immunity  of  the  whole  body.  Haubner 
calculates  that  the  mortality  from  the  inoculation  is  from  i  to 
2  per  cent  and  that  the  tips  of  the  tails  are  lost  in  from  5  to  10 
per  cent  of  the  cases.  In  Holland,  among  59,180  cattle 
inoculated  in  1S78  and  1879,  the  mortality  amounted  to  only 
0.66  per  cent. 

The  opponents  of  inoculation,  among  whom  we  may  men- 


302  FOOT    AND    MOUTH    DISEASE 

tion  Rolof,  Ziindel,  Kitt,  M'Fadyean  and  others,  assert  that  up 
to  the  present  no  positive  case  of  immunity  has  been  proved  to 
have  been  obtained  from  inoculation.  They  also  point  to  the 
fact  that  even  the  advocates  for  inoculation  are  unable  to  give 
the  exact  duration  of  the  immunity  and  consequenth'  make 
several  inoculations.  The  specific  nature  of  the  tumor  pro- 
duced by  inoculation  is  disputed,  because  an  exactly  similar 
tumor  appears  after  the  inoculation  of  pus  or  milk.  We  must 
also  bear  in  mind  that  in  those  countries  in  which  inoculation 
has  been  most  practiced,  the  disease  shows  no  decrease,  as  for 
instance  in  England,  where  the  official  report  lays  particular 
stress  on  the  doubtful  value  of  obligatory  inoculation  for  pleuro- 
pneumonia as  in  France  and  Belgium  where  inoculation  was 
obligator3^  The  best  procedure  seems  to  be  stamping  out 
the  disease  with  thorough  disinfection  or  destruction  by  fire  of 
all  infected  sheds  and  barns.  The  success  of  this  method  is 
illustrated  by  the  eradication  of  the  disease  from  the  United 
States. 

REFERENCES. 

1.  NocARD    AND    Roux.        Le     microbe    de    la    peripneumonie. 
Recueil  de  Med.  Veterinaire.     March  24,  1898.     p.  213.     [Ttans.  in  The 

Veterinary  Journal,  London.     Vol.  XLVII.     (1898).     p.  147. 

2.  Salmon.     Annual  Reports  of  the  Bureau  of  Animal  Industry. 
1884-1892. 

3.  Smith.     Annual  Report  of  the  Bureau  of  Animal  Industry. 
1895-6.     p.  143. 

4.  WallEy.     The  four  bovine  scourges.     (1S79). 


FOOT  AND  MOUTH  DISEASE. 

Synonyms.  Eczema  epizootica  ;  epizootic  aphtha  ;  vesi- 
cula  aphtha  ;   vesicular  epizootic  ;  apthous  fever  ;  murrain. 

§  226.  Characterization.  Foot  and  mouth  disease  is  a 
highly  infectious  disease  of  animals.  It  is  determined  by  the 
eruption  of  vesicles  in  the  mouth,  around  the  coronet  of  the 
foot  and  between  the  toes.  It  is  said  to  be  more  common 
among  cattle  but  swine  are  quite  susceptible  ;  sheep,  goats, 
horses,  dogs,  cats  and  fowls  are  sometimes  attacked.  The 
human    species   is   also   susceptible   and    may  be  infected  hy 


ETIOLOGY  303 

drinking    the    unboiled    milk  of  animals   suffering    from    the 
disease.     The  mortality  is  not  high. 

§  227.  History.  Foot  and  mouth  disea.se  was  quite 
accurately  described  in  the  eighteenth  century.  Very  destruc- 
tive outbreaks  are  reported  in  1809  and  in  the  early  part  of  the 
nineteenth  century  it  was  the  source  of  much  loss  in  southern 
Europe.  In  1883,  Great  Britain  lost  heavily  from  its  ravages. 
In  1892,  Prussia  is  reported  to  have  had  8,000,000  cattle 
affected.  It  was  during  the  years  1S90  and  1893  that  the  last 
severe  epizootic  appeared  in  Germany. 

§  228.  Geographical  distribution.  This  disease  seems 
to  be  very  largel}-  restricted  to  Europe  although  it  is  alleged 
to  have  been  introduced  into  almost  every  cattle  raising  coun- 
try. Its  invasion  into  the  United  States  has  been  prevented 
by  the  enforcement  of  rigid  quarantine  measures. 

§  229.  Etiology.  The  specific  cause  of  foot  and  mouth 
disease  has  not  been  clearly  demonstrated.  It  is  generally 
believed,  however,  that  it  is  caused  by  a  specific  infection  and 
that  every  outbreak  starts  from  some  previous  case  or  cases. 
The  virus  is  contained  in  the  eruptions  and  given  off  from  the 
mouth  and  feet  causing  its  wide  distribution.  Animals  may 
be  infected  directly  bj-  coming  in  contact  with  the  disease,  or 
indirectly  by  being  exposed  to  the  virus  in  stables,  cars  or 
other  places  recently  occupied  by  infected  animals.  It  is  stated 
that  the  virus  is  destroyed  in  a  short  time  by  drying,  but  some 
writers  maintain  that  it  will  persist  for  several  months. 
Animals  that  have  passed  through  the  disease  may  carry  the 
virus  for  several  months.  The  infected  matter  may  be  carried  on 
the  clothing  or  hands  of  human  beings  and  thus  be  transmitted 
to  animals  or  men.      Milk  is  often  the  carrier  of  the  virus. 

§  230.  Symptoms.  The  symptoms  of  foot  and  mouth 
disease  vary  greatly  in  different  epizootics,  sometimes  they  are 
quite  mild  and  at  others  very  severe.  The  first  evidence  of  the 
disease  is  a  rise  of  temperature  which  in  cattle  rarely  exceeds 
104°  F.  This  follows  after  a  period  of  incubation  of  from  3  to 
5  days  although  in  rare  cases  it  may  be  shorter  or  longer  than 
these  limits.  The  mucous  membrane  of  the  mouth  becomes 
reddened,  the  appetite  is  diminished,  and  rumination  ceases. 


304  FOOT    AND    MOUTH    DISEASE 

The  mouth  is  usually  kept  closed  and  the  quantity  of  saliva  is 
increased.  A  smacking  sound  is  not  infrequently  made  by  the 
animal.  These  symptoms  are  chiefly  due  to  the  pain  accom- 
panying the  disease  in  the  mouth.  After  two  or  three  days 
the  eruption  appears.  This  consists  of  small  yellowish-white 
vesicles  or  blisters  varying  in  size  from  a  hemp  seed  to  a  pea 
•on  the  gums  and  inner  surface  of  the  lips,  the  inside  of  the 
cheeks,  the  border  and  under  the  surface  of  the  tongue.  They 
may  become  half  an  inch  or  more  in  diameter.  In  some  cases 
the  back  of  the  tongue  near  the  tip  may  be  the  seat  of  large 
blisters. 

These  vesicles  burst  soon  after  their  appearance,  some- 
times on  the  first  day.  More  rarely  they  may  persist  for  two 
or  three  days.  After  they  have  ruptured  the  greyish-white 
membrane  forming  the  blister  may  remain  for  a  day  or  more 
■or  disappear  speedily  and  leave  deeply  reddened  areas  or 
erosions  which  are  very  painful.  These  exposed  areas  may 
soon  become  covered  again  with  the  normal  epithelium  or  they 
may  be  converted  into  ulcers.  In  this  stage  the  .saliva  forms 
in  large  quantities  and  hangs  in  strings  from  the  mouth.  In 
eight  to  fourteen  days  the  disease  may  have  entirely  disap- 
peared. 

In  addition  to  the  changes  in  the  mouth,  one  or  more  feet 
may  become  diseased.  The  skin  around  the  coronet  and  in 
the  cleft  between  the  toes  becomes  hot  and  tender  and  may 
swell.  Blisters  appear  as  in  the  mouth,  but  they  are  speedily 
ruptured  and  the  inflamed,  exposed  areas  are  covered  with  a 
viscid  exudate. 

The  udder,  more  particularly  the  teats,  may  be  the  seat 
of  lesions.  Some  authorities  regard  the  udder  disease  merely 
at  she  result  of  infection  during  milking.  The  vesicles  are 
broken  as  they  appear  by  the  hands  of  the  milker  and  the 
teats  become  covered  with  reddened  areas,  deprived  of  the 
superficial  layer  of  the  skin  and  are  very  tender.  The  heal- 
ing, however,  goes  on  quite  rapidly.  The  milk  is  said  to  be 
somewhat  changed  in  appearance  and  unfit  for  making  butter 
or  cheese.  These  are  the  main  symptoms  accompanying  the 
uncomplicated  cases  of  foot  and  mouth  disease.    In  all  such  cases 


MORBID    ANATOMY  305 

recovery  is  usually  rapid  and  complete.  In  certain  other  cases, 
however,  complications  arise  which  are  not  only  injurious  but 
may  be  fatal.  Thus  the  mouth  lesions  may  be  accompanied 
by  nasal  catarrh  or  pneumonia.  The  feet  may  become  very 
much  swollen  and  the  inflammation  and  suppuration  extend 
to  the  tendons  and  bones  resulting  in  the  loss  of  the  hoof. 
Such  cases  are  usually  fatal.  As  a  result  of  the  general  affec- 
tion young  calves  may  succumb  to  a  secondar}^  inflammation 
of  the  stomach  and  bowels  and  older  animals  maj-  abort  or 
suffer  from  inflammation  of  the  udder. 

The  duration  of  the  disease  in  uncomplicated  cases  varies 
from  10  to  20  days.  Where  complications  occur  either  with 
the  regular  course  or  as  sequelae  the  duration  becomes  in- 
definite. The  mortalit}-  varies  with  the  severity  of  the 
attacks,  the  age  and  condition  of  the  animals  and  the  treat- 
ment. Ordinarily  the  mortality  is  not  high  excepting  in  very 
young  animals. 

§  231.  Morbid  anatomy.  The  tissue  changes  found  at 
post  mortem  vary  to  a  marked  degree.  There  is  in  certain 
cases  hyperaemia  and  oedma,  catarrh  of  the  nares  and  mucosa 
of  the  lungs  and  dilatation  of  the  heart.  There  may  be  fatty 
degeneration  and  hemorrhagic  infarcts  in  the  heart  muscle. 
In  other  cases  there  is  severe  gastro-enteritis  with  intestinal 
hemorrhage.  In  the  stomachs  of  cattle  oval  reddish  areas 
which  ultimately  form  ulcers  appear.  These  often  become 
confluent.  The  involved  portion  of  the  mucous  membrane 
becomes  thickened.  The  areas  of  necrotic  tissue  in  which  the 
ulcers  appear  become  surrounded  by  a  reddish  line  of  demar- 
cation which,  in  the  healing  process,  forms  a  cicatrix. 
The  lesions  on  the  mucous  membrane  rarelj'  extend  deeper 
than  the  mucosa.  Ulcers  of  a  nature  similar  to  those  found 
in  the  stomach  occur  in  the  intestines.  On  the  feet  inflam- 
mations may  follow  the  simple  vesicles  about  the  coronet. 
These  may  extend  deep  into  the  tissues,  pass  under  the  hoof 
and  cause  it  to  slough  off,  extend  into  the  bone  producing 
necrosis  or  permanent  arthritis.  It  is  stated  b}^  some  authori- 
ties that  in  the  mild  non-fatal  cases  the  obvious  lesions  are  so 
slight  that  frequently  they  escape  notice.  In  sheep  and  swine 
the  lesions  are  more  frequently  restricted  to  the  feet. 


306  RABIES 

§  232.  Differential  diagnosis.  Foot  and  mouth  disease 
must  be  differentiated  from  (i)  various  forms  of  stomatitis 
caused  by  different  fungi  and  often  referred  to  as  sporadic 
aphthae,  (2)  from  stomatitis  due  to  drugs  and  injuries,  (3) 
from  actinomycosis  of  the  tongue  and  (4)  from  variola.  It 
must  also  be  differentiated  from  simple  cellulitis,  often  of 
streptococcic  origin,  in  the  subcutaneous  tissue  about  the 
coronet  and  from  the  sloughing  of  the  hoof  resulting  from  the 
extension  of  the  inflammatory  process  and  from  eczemas  due 
to  dietary  causes.  The  means  of  differentiating  these  must  be 
found  largely  in  the  history  of  the  cases  and  in  the  study  of 
the  nature  of  the  lesions  themselves. 

§233.  Prevention.  Preventive  inoculations  do  not  seem 
to  have  given  satisfactory  results.  The  isolating  of  the  diseased 
animal  and  the  placing  of  the  well  ones  in  non-infected  fields 
and  stables  tend  very  largely  to  the  checking  of  the  spread  of  the 
disease.  The  milk  of  the  diseased  animal  should  be  sterilized 
before  it  is  used. 

REFERENCES. 
Wai.i,EY.     The  Four  Bovine  Scourges.     1879.     p.  61. 


RABIES. 


Synonyms.     Hydrophobia  ;  canine  madness. 

§  234.  Characterization.  Rabies  is  an  acute  infectious 
disease  transmitted  from  animal  to  animal  or  from  animal  to 
man  by  the  bite  of  the  rabid  individual  or  by  direct  inocula- 
tion. It  is  not  known  to  be  contracted  or  transmitted  in  any 
other  manner.  It  is  characterized  by  a  long  and  variable 
period  of  incubation,  followed  by  symptoms  referable  to  the 
nervous  system  lasting  from  one  to  ten  days  ending  in  paralysis 
and  death,  without  recognizable  gross  anatomical  changes. 

The  dog  is  the  animal  most  commonly  affected  although 
all  of  the  canine  and  feline  races  seem  to  suffer  from  rabies 
more  than  other  species.  All  warm  blooded  animals  appear  to 
be  susceptible.  It  is  a  serious  disease  in  man,  cattle,  sheep, 
horses  and  swine.     An  explanation  for  its  greater  frequency 


HISTORY  307 

among  dogs  is  found  in  their  tendency  to  bite.  A  very  large 
percentage,  in  fact  nearly  all,  of  the  cases  in  man  and  in  the 
domesticated  animals  are  caused  by  inoculation  from  the  bites 
of  rabid  dogs. 

§  235.  History.  Rabies  was  described  by  Aristotle  in 
the  fourth  century  B.  C.  He  wrote,  "Dogs  suffer  from  mad- 
ness that  puts  them  in  a  state  of  fury,  and  all  the  animals  that 
they  bite,  when  in  this  condition,  become  also  attacked  by 
rabies."  Cornelius  Celsius  who  lived  in  the  first  part  of  the 
Christian  era  seems  to  have  been  the  first  to  refer  to  human 
rabies  and  to  employ  the  term  "hydrophobia." 

The  transmission  of  the  disease  by  wolves  to  man  was 
recorded  in  1591.  In  1803,  and  for  a  number  of  years  follow- 
ing, it  was  epizootic  among  foxes  in  Southern  Germany  and 
Switzerland. 

During  the  latter  part  of  the  eighteenth  and  the  beginning 
of  the  nineteenth  century  the  disease  extended  over  Europe 
and  about  this  time  it  appeared  in  America.  The  first  out- 
break in  this  country  was  reported  from  Boston  in  1768.  In 
1770  to  1 77 1  it  was  observed  in  dogs  and  foxes  in  the  vicinity 
of  Boston  ;  in  the  year  1779  it  appeared  in  Philadelphia  and 
in  the  state  of  Maryland  :  in  1785  it  was  prevalent  throughout 
the  northern  States  and  soon  after  it  spread  to  the  southern 
States.  During  the  last  century  it  has  caused  heavy  losses 
among  farm  animals  throughout  Europe  and  America. 

It  has  called  forth  careful  study  from  many  of  the  ablest 
men  in  the  medical  professions.  Among  them  may  be  men- 
tioned John  Hunter  in  England,  Viborg  in  Copenhagen,  Wal- 
dinger  in  Vienna,  Hertwig  in  Germany  and  Pasteur  in  France. 
Without  detracting  in  the  least  from  the  great  work  of  other 
investigators,  we  may  say  that  to  Pasteur  and  his  co-laborers, 
Nocard  and  Roux,  we  owe  much  of  the  knowledge  which  we 
possess  of  the  disease  at  the  present  day. 

§236.  Geographical  distribution.  Rabies  is  known 
to  exist  in  almost  every  country  on  the  globe.  Australia  is 
the  only  land  which  is  said  to  be  absolutely  free  from  it.  This 
exemption  is  the  gratifying  result  of  a  rigid  quarantine  en- 
forced against  dogs  imported  to  that  island.       Rabies  is  very 


3o8  RABIES 

common  in  France,  Belgium  and  Russia.  In  the  latter 
country  it  is  perhaps  more  often  seen  in  wolves  than  in  any 
other  part  of  the  world.  In  Holland,  Denmark  and  Sweden 
it  is  very  rare.  In  England,  it  has  from  time  to  time  been 
widespread,  but  at  present  it  is  practically  eradicated.  Sal- 
mon has  found  that  rabies  exists  in  nearly  every  part  of  the 
United  States. 

Inquiries  which  the  writer  has  made  during  the  last  few 
years,  by  verifying  current  newspaper  reports  of  rabies,  shows 
that  the  larger  number  of  cases  come  from  certain  districts  in 
which  the  disease  seems  to  have  become  established.  Newh^ 
infected  districts  are  constantl}'  springing  up,  due  presumably 
to  the  introduction  in  some  manner  of  an  infected  dog. 

The  prevalence  of  the  disease  cannot  be  accurately  deter- 
mined as  there  are  no  reliable  statistics  concerning  it. 
Ravenel  has  reported  that  the  State  Live  Stock  Sanitary  Board 
of  Pennsylvania  has  investigated  82  cases  of  rabies  since  1897. 
Of  these  there  were  58  dogs,  4  horses,  17  cows,  i  cat  and  2 
human  beings.  Since  November  1900  the  New  York  State 
Veterinary  College  has  investigated  27  cases  of  rabies  of  which 
14  were  in  dogs,  9  in  cattle,  i  in  horses,  i  in  sheep  and  two  in 
men.  Salmon  states  that  in  the  District  of  Columbia  from 
1893  to  August  1900  rabies  has  been  positively  diagnosed  in 
animals  in  91  cases.  These  consist  of  80  dogs,  5  cows,  2 
horses,  2  foxes  and  2  cats.  In  addition  to  these  the  records  of 
the  health  department  of  the  District  of  Columbia  show  that 
since  1874  there  has  been  in  the  human  species  seven  deaths 
from  rabies.  These  illustrations  from  the  experiences  of  a  few 
laboratories  could  be  duplicated  from  the  records  of  many 
others. 

In  Europe  the  disease  seems  to  be  more  prevalent.  In 
1898  the  official  reports  show  1,202  cases  of  rabies  in  animals 
(mostly  dogs)  in  German}'.  In  1899,  2,374  rabid  animals 
were  reported  from  France  and  444  cases  from  Belgium. 

§  237.  Etiology.  Although  rabies  has  become  recog- 
nized as  a  specific  disease,  its  primar}'  etiological  factor  has 
not  been  isolated  or  found.  It  is  known  that  it  exist  in  the 
brain,  spinal  cord  and  saliva  of  the  affected  animal.     In  cer- 


METHOD    OF    INVASION  309 

tain  instances  its  presence  has  been  reported  in  salivary  glands, 
the  pancreas  and  milk.  It  has  not  been  found  in  the  blood. 
A  very  large  amount  of  work  has  been  done  by  way  of  investi- 
gation to  determine,  if  possible,  the  nature  of  the  specific 
cause  but  thus  far  positive  results  have  not  been  recorded.  It 
should  be  stated,  however,  that  a  number  of  workers  have 
found  in  the  brain  or  cord  of  affected  animals  various  forms  of 
bacteria  and  Blastomycetes  but  in  every  instance  the  conclusions 
reached  b}^  the  authors  have  not  been  confirmed  by  others. 
While  it  is  true  that  the  cause  has  not  been  recognized,  the 
researches  in  recent  times  have  brought  to  our  knowledge 
many  facts  concerning  it.  It  can  be  removed  from  the  saliva 
by  filtration  which  indicates  that  it  is  a  solid  particle. 

§  238.  Method  of  invasion.  When  introduced  into  an 
animal  either  experimentally  or  by  the  bite  of  a  rabid  dog,  the 
virus  remains  for  a  time  without  producing  either  local  or 
general  symptoms.  The  period  of  incubation  varies  within 
quite  wide  limits.  The  virus  penetrates  the  nervous  system, 
by  following  the  nerve  trunks  from  the  site  of  infection  to  the 
spinal  cord,  then  through  the  spinal  cord  to  the  brain.  This 
has  been  proven  by  inoculating  an  animal  in  one  of  its  legs 
with  virulent  material.  After  a  suitable  time,  but  before  the 
symptoms  of  rabies  appear,  the  virus  will  be  found,  on  killing 
the  animal,  in  the  nerves  of  the  limb,  and  even  in  the  part  of 
the  spinal  cord  into  which  the  nerve  enters,  while  the  upper 
part  of  the  cord  and  the  brain  are  still  uninfected.  This  ex- 
plains the  fact  why  the  earliest  symptoms,  both  in  man  and  ani- 
mals, such  as  itching,  tingling,  numbness  and  other  nervous 
sensations,  often  appear  in  the  part  of  the  body  which  received' 
the  virus.  In  the  case  of  a  bite  about  the  face  and  head  the 
route  along  the  nerve  to  the  central  nervous  system  is  much, 
shorter.  While  the  nerves  seem  to  form  the  main  route  by 
which  the  virus  travels,  the  circulation  may  at  times  assist, 
especially  in  small  animals.  Inoculation  into  the  large  nerve 
of  the  leg  is  almost  as  certain  to  produce  the  disease,  as  inocu- 
lation directly  into  the  sub-dural  space,  while  injection  beneath, 
the  skin  of  the  leg  is  not  so  sure. 

Resistance  of  the  virus.   The  action  of  the  virus  is  destroyed 


3IO  RABIES 

by  drying  and  by  the  action  of  light.  In  dry  air,  protected 
from  light  and  putrefaction,  the  virulence  of  the  spinal  cord  of 
rabbits  is  destroyed  in  fourteen  to  fifteen  days.  When  spread 
in  thin  layers  it  is  entirel}-  destroyed  by  drying  in  from  four  to 
five  days.  Sunlight  destroys  it  in  about  fort}-  hours.  The 
loss  of  virulence  by  drying  is  gradual  but  quite  regular,  which 
fact  was  taken  advantage  of  by  Pasteur  in  the  preparation  of  his 
vaccine.  The  virus  may  be  preserved  in  neutral  glycerin  at 
ordinary  temperature  for  a  long  time.  Roux  found  that  after 
four  weeks  in  glycerin  at  30°  C,  the  virus  in  a  rabid  brain 
had  the  same  power  as  w^hen  perfecth-  fresh.  The  writer  has 
found  that  rabbits  inoculated  with  rabid  brains  that  had  been 
kept  in  glycerin  from  three  to  four  weeks  did  not  develop  the 
disease  as  quickh'  as  when  they  were  inoculated  with  the 
freshly  removed  brain. 

It  is  quite  resistant  to  putrefaction.  Galtier  has  found 
the  virus  active  in  the  central  nervous  system  of  rabbits  buried 
for  twenty-three  days,  of  sheep  buried  thirt3'-one  days  and  of 
dogs  buried  forty-four  days.  Other  observers  have  found  it 
still  active  in  animals  buried  for  twenty-four  days. 

It  is  destroyed  completely  by  a  temperature  of  50°  C.  in 
one  hour  or  60°  C.  in  one-half  hour.  It  is  uninjured  by 
exposure  to  extreme  cold,  resisting  the  prolonged  application 
of  a  temperature  from  10  to  20°  C.  below  zero. 

Its  activity  is  de.stroyed  in  one  hour  b}-  a  five  per  cent 
solution  of  carbolic  acid,  or  by  a  i  to  1,000  solution  of  corro- 
sive sublimate.  Water  saturated  with  iodine  destro}-es  it  in 
ten  minutes. 

§  239.  Period  of  incubation.  The  period  of  incuba- 
tion is  quite  variable  depending  on  the  site  of  the  wound 
which  is  almost  always  a  bite,  the  amount  of  virus  introduced 
and  its  virulence.  In  general  it  may  be  said  for  all  animals 
that  the  period  of  incubation  seldom  exceeds  sixty  days, 
though  in  man  and  in  some  of  the  larger  animals,  it  some- 
times, though  very  rarely  reaches  one  year.  A  few  cases  of  a 
longer  period  have  been  reported.  The  average  period  as 
given  b}-  Ravenel  is  as  follows  : 

In  man,  40  da^'S. 


PERIOD    OF    INCUBATION 


311 


In  dogs,  21  to  40  da3^s. 

lu  horses,  28  to  56  days. 

In  cows,  28  to  56  da^'S. 

In  cats,  14  to  28  days. 

In  pigs,  14  to  21  days. 

In  goats  and  sheep,  21  to  28  days. 

In  birds,  14  to  40  days. 

In  rabbits  inoculated  subdurally  with  the  brain  from  rabid 
animals,  the  writer  has  found  the  period  of  incubation  to  vary 
from  12  to  62  days  and  the  duration  of  the  disease  to  range 
from  a  few  hours  to  three  days.  Wesbrook  reports  a  period  of 
incubation  in  rabbits  to  extend  in  one  case  over  a  hundred 
days.  In  the  disease  as  it  is  naturally  contracted  from  the 
bites  of  rabid  animals,  the  period  of  incubation  varies  with 
reference  to  the  location  and  extent  of  the  bites.  If  the  indi- 
vidual is  bitten  about  the  head  the  period  of  incubation  is 
much  shorter  than  if  the  injuries  are  on  the  extremities. 

In  the  dog,  the  period  of  incubation  in  144  cases  was 
clearly  determined  by  Peuch.  His  table  with  the  addition  of 
percentages  is  appended. 

PERIOD   OF   INCUBATION    OF   RABIES   IN   THE   DOG. 


Number  of  davs  of 

Number  of 

.     - 

Per  cent. 

incubation. 

cases. 

5  to 

10 

3 

2.08 

10  to 

15 

8 

5  55 

15  to 

20 

13 

903 

20  to 

25 

25 

17-36 

25  to 

30 

13 

903 

30  to 

35 

25 

17-36 

35  to 

40 

6 

4.17 

40  to 

45 

II 

7.64 

45  to 

50 

9 

6.25 

50  to 

55 

4 

2.78 

55  to 

60 

2 

1-39 

60  to 

65 

7 

4.86 

65  to 

70 

I 

.69 

70  to 

75 

5 

3-47 

80  to 

90 

7 

4.86 

100  to 

120 

4 

2.78 

365  - 

tal 

I 

.69 

To 

144 

312 


RABIES 


The  somewhat  popular  opinion  that  most  of  the  cases  of 
rabies  occur  in  the  summer,  especially  in  "  dog  days",  is  not 
founded  upon  facts.  Rabid  dogs  are  nearly  if  not  quite  as 
numerous  in  winter  as  in  summer.  Salmon  has  collected 
14,066  cases  of  rabies  in  dogs  with  the  months  the  disease 
occurred.  The  results  are  exceedingly  interesting  as  the  ap- 
pended table  shows. 

CASES  OF   RABIES   IN   DOGS,  BY   MONTHS. 


Source 

5  "^ 

pr. 

a 

CI 

>. 

M 

> 

0 

d 
III 

0 

►—1 

fe 

'^ 

< 
32 

32 

1—1 
42 

>— 1 
32 

< 



30 

XT. 

35 

0 

41 

24 

32 

Bourrel 

36 

31 

26 

393 

St.  Cvr  ... 

12   15 

6 

15 

13 

7 

4 

9 

I 

3 



2 

87 

Hogyes 

309  3io;3i4 

367 

450 

502 

508 

537 

455 

438 

303 

396 

4961 

Leblanc 

103   97,121 

192 

155 

138 

147 

123 

104 

117 

95 

100 

1492 

France 

: 

1895 

89  155,153 

184 

181 

129 

157 

147 

133 

no 

105 

149 

1692 

1896 

124  I38115I 

150 

147 

199 

138 

117 

131 

125 

103 

164 

1687 

1897 

131   1511189 

202 

225 

172 

192 

154 

136 

131 

150 

140 

1973 

1898 

139  148--- 

181 
1323 

216 
I419 

278 
1467 

185 
1435 

177 
1294 

150 

153 

154 

1781 

Total 

943 

1045 

960 

1 145 

965 

933 

"37 

14066 

§  240.  Symptoms.  Rabies  is  generally  divided  into  two 
forms,  furious  and  dumb  rabies.  In  the  first  the  animal  is  irri- 
table, aggressive  and  bites  nearly  every  object  which  comes  in 
its  way  ;  in  the  second  the  muscles  of  its  jaw  are  paralyzed 
almost  from  the  beginning  and  being  unable  to  bite,  the  animal 
remains  more  quiet  and  tranquil.  Essentially  the  two  forms 
of  the  disease  are  the  same,  but  probably  owing  to  the  parts 
of  the  brain  attacked  or  the  acuteness  of  the  attack  or  both, 
paralysis  appears  much  sooner  in  the  dumb  form  than  in  the 
other.  The  saliva  from  a  case  of  dumb  rabies  is  just  as 
dangerous  and  virulent  as  that  from  a  case  of  furious  rabies. 
Dogs  affected  with  dumb  rabies  are  less  dangerous  simph' 
because  they  are  unable  to  bite  and  thus  to  infect  others. 

Dumb  rabies  and  furious  rabies  do  not  always  represent 
two  distinct  types  of  disease.  The  typical  cases  belong  to  the 
two  extremes  of  symptoms  and  there  are  always  gradations 
between  them.     In  fact,  almost  every  case  of  furious  rabies 


SYMPTOMS  313 

sooner  or  later  changes  to  the  dumb  form,  that  is,  the  final 
stage  of  the  disease  is  ahnost  invariably  paralj^tic.  In  the 
typical  development  of  the  dumb  form,  the  paralysis  occurs  on 
the  first  day  of  the  disease.  It  may  not  appear,  however, 
until  the  second  or  third  or  even  a  later  day. 

Again,  a  dog  does  not  necessarily  bite  everything  about  it 
even  if  it  has  rabies  and  its  jaws  are  not  paralyzed.  It  may  be 
combative  and  furious  all  of  the  time  or  only  part  of  the  time, 
or  not  at  all.  There  is  perhaps  no  disease  in  which  the  symp- 
toms may  vary  more  than  in  rabies  of  the  dog. 

Furious  rabies.  The  symptoms  appear  very  gradually. 
The  animal's  habits  and  behavior  are  changed.  It  may  be 
more  restless  or  affectionate  than  usual,  seeking  to  be  near  its 
master  or  mistress,  fawning,  licking  the  hand  or  face  and 
apparently  seeking  sympathy  or  assistance.  Such  caresses 
are,  however,  extremely  dangerous,  for  the  animal's  tongue, 
moist  with  virulent  saliva,  coming  in  contact  with  a  part 
where  the  skin  is  thin,  abraded  or  wounded  may  fatally  infect 
the  person  to  whom  it  is  endeavoring  to  demonstrate  its  affec- 
tion. The  reported  cases  in  which  rabies  has  developed  from 
such  inoculations  are  quite  numerous. 

In  most  cases  dogs  first  become  dull,  gloomy,  morose, 
seeking  solitude  and  isolation  in  out-of-the-way  places  or  retir- 
ing under  pieces  of  furniture.  But  in  their  retirement  they 
cannot  rest,  they  are  uneasy  and  agitated,  they  lie  down  and 
assume  the  attitude  of  repose,  but  in  a  few  minutes  they  are 
up  walking  about  "seeking  rest,  but  finding  none."  Occa- 
sionally this  restlessness  may  disappear  for  a  time  and  the 
animal  becomes  lively  and  affectionate  ;  oftener  it  sinks  into  a 
sullen  gloominess  from  which  even  its  master's  voice  rouses  it 
but  temporarily.  At  this  period  dogs  may  have  aberrations  of 
the  senses  which  cause  hallucinations  and  lead  them  to  think 
they  are  being  annoyed  by  something  or  that  some  animal  or 
person  is  endeavoring  to  injure  them.  They  crouch  ready  ta 
spring  upon  the  enemy  ;  they  rush  forward  and  snap  at  the 
air  ;  they  throw  themselves,  howling  and  furious,  against  the 
wall  as  though  they  heard  sounds  beyond  it. 


314  RABIES 

While  at  first  the  affected  dog  may  not  be  disposed  to  bite, 
it  becomes  more  dangerous  as  its  hallucinations  and  delirium 
increase. 

The  disturbance  of  the  sensations  leads  to  chills  and  itch- 
ing. If  the  place  where  the  bite  occurred  is  accessible,  the 
dog  licks  the  scar  and  later  bites  and  tears  the  tissues.  In 
this  case  it  bites  into  its  own  flesh  with  apparent  pleasure  and 
'Satisfaction.  Food  is  taken  until  the  disease  is  considerably 
advanced,  if  it  is  something  which  can  be  swallowed  without 
mastication,  otherwise  it  is  soon  dropped.  Difficulty  in  swal- 
lowing is  an  early  s^'mptom.  Mad  dogs  have  no  fear  or  dread 
of  water,  they  continue  to  drink  until  paralysis  prevents  them 
from  swallowing. 

When  the  furious  symptoms  appear,  the  dog  leaves  his 
home  and  starts  upon  a  long  chase  with  no  apparent  object  in 
view  other  than  to  be  traveling.  He  trots  at  a  rapid  pace,  eye 
haggard  and  tail  depressed.  He  is  indifferent  to  the  sur-- 
roundings.  He  flies  at  and  bites  persons  w^hom  he  meets,  but 
usually  does  not  apparently  search  for  them  or  even  notice 
them  if  they  remain  quiet.  Dogs  in  this  condition  may  travel 
many  miles  and  finally  drop  from  exhaustion  and  die.  Often 
after  the  absence  of  a  day  or  two  they  return  to  their  home, 
exhausted,  emaciated,  covered  with  dust,  thus  presenting  a 
most  forlorn  and  miserable  appearance.  Those  who  have  pity 
for  such  an  animal  and  try  to  make  it  clean  and  comfortable 
are  in  great  danger  of  being  bitten  as  the  disease  has  advanced 
to  a  point  where  the  delirium  or  insanitj^  is  most  marked  and 
where  a  treacherous  bite  is  most  common. 

If  the  animal,  instead  of  being  allowed  to  escape,  is  kept 
confined,  the  paroxysms  of  fury  are  seen  to  occur  intermit- 
tently or,  in  the  absence  of  provocation,  they  may  be  entirely 
wanting.  If  excited  it  howls,  rushes  upon  objects  that  are 
thrust  toward  it  or  throws  itself  against  the  bars  of  its  cage 
and  bites  with  great  fury. 

As  death  approaches  the  animal  becomes  exhausted  and  is 
scarcely  able  to  .stand.  The  eyes  are  dull  and  sunken  and  the 
expression  is  that  of  pain  and  despair.  Paralysis  appears  in 
the  jaws  or  in  the  posterior  extremities  and  extends  rapidly  to 


MORBID    ANATOMY     .  315 

Other  parts  of  the  body.  The  animal,  being  unable  to  stand, 
lies  extended  upon  its  side,  the  respiration  becoming  more  and 
more  difficult.  There  are  spasmodic  contractions  of  certain 
groups  of  muscles,  complete  prostration  and  finally  death. 

The  ordinary  course  of  the  disease  is  four  or  five  days.  It 
may  be  as  short  as  two  or  as  long  as  ten  days. 

Dumb  rabies.  When  this  form  of  the  disease  is  typical,  it 
comes  on  with  restlessness,  depression,  a  tendency  to  lick 
objects  and  paralysis  of  the  muscles  which  close  the  jaws.  As 
a  consequence  of  the  paralysis,  the  lower  jaw  drops,  the  animal 
is  unable  to  close  the  mouth,  the  tongue  hangs  out  and  an 
abundance  of  saliva  escapes.  The  mucous  membrane  of  the 
mouth  becomes  dry,  discolored  and  covered  with  dust.  The 
animal  remains  quiet,  it  does  not  respond  to  calls  and  appears 
to  understand  its  helplessness.  Bouley  states  that  the  animal 
cannot  bite  and  does  not  desire  to  bite.  When  dum.b  rabies 
follows  a  period  in  which  the  animal  has  been  affected  with  the 
furious  form,  the  desire  and  tendency  to  bite  may  be  retained 
even  after  the  jaw  is  paralyzed. 

The  course  of  the  disease  is  short,  death  usualh'  occurring 
in  from  two  to  four  days. 

§  241.  Morbid  anatomy.  One  of  the  striking  char- 
acteristics of  rabies  is  the  absence  of  constant,  recognizable 
lesions.  The  mucosa  of  the  pharynx  and  larynx  are  con- 
gested. The  spleen  is  sometimes  enlarged  and  dark  colored. 
In  dogs  the  stomach  often  contains  a  variety  of  foreign  matter 
such  as  earth,  stones,  pieces  of  iron,  bits  of  leather,  wood,  etc. 
x-Vxe  reports  finding  such  foreign  substances  present  in  90  per 
cent  of  200  cases  he  examined.  Galtier  reports  such  findings 
in  from  50  to  70  per  cent.  In  experimental  animals  and  cattle 
the  writer  has  rarely  found  them.  It  seems  to  be  true  that 
the  obvious  lesions  are  not  constant  and  it  is  very  likel}'  that 
the  pronounced  changes  occasionally  found  in  a  single  organ 
are  accidental  or  secondary  rather  than  primarily  related 
to  the  disease.  The  lesions  in  the  brain  and  spinal  cord  are 
likewise  variable.  In  some  cases  there  is  a  marked  hyperemia, 
while  in  others  the  brain  appears  to  be  normal. 


3l6  RABIES 

Certain  investigators  however  have  found  histological 
•changes,  which  to  their  minds  have  been  pathognomonic  of  the 
disease.  The  close  simulation  of  the  nervous  lesions  to  those 
due  to  other  diseases,  and  the  possibility  of  greater  or  less  post- 
mortem changes  will  foster  an  element  of  doubt  in  the  minds 
-of  the  majority  of  working  histologists.  This  doubt  instead 
of  diminishing  shows  a  tendency  to  grow  when  a  review  is 
taken  of  the  conflicting  results  and  opinions  held  by  those  who 
have  already  investigated  this  field.  It  also  appears  that  some 
portions  of  the  nervous  system  may  exhibit  lesions  of  a  pro- 
nounced character,  other  portions  very  slightly,  and  still 
others  none  at  all,  thus  presenting  additional  difficulties. 

One  of  the  most  common  lesions  that  has  been  observed  is 
of  an  inflammatory  character,  the  congested  blood  vessels  fre- 
quentl}'  showing  diapedesis  and,  according  to  some,  a  perivas- 
cular exudation  of  a  granular  or  hvaline  substance.  HvDere- 
mia  and  lymph-stasis,  although  of  not  so  much  significance 
when  taken  bj'  themselves,  have  been  taken  into  considera- 
tion along  with  other  changes.  The  blood  vessels  quite  as 
much  or  even  more  than  the  nerve  structures  have  been  noted 
as  the  locus  of  some  of  the  most  marked  changes,  among 
which  are  the  proliferation  of  the  epithelial  cells  and  of  the 
connective  tissue  elements  of  the  outer  coat,  with  the  infiltra- 
tion by  lymphoid  cells.  Such  lesions  may  be  nodular  pri- 
marily, but  later  become  diffuse.  The  inflammatorj^  proces- 
ses may  progress  to  such  an  extent  as  to  obliterate  certain 
vessels. 

Pathological  miliar}'  centers  have  been  noted  not  only  in 
the  axial  portions  of  the  nervous  sj'Stem,  but  in  the  gray 
matter  as  well.  These  centers  are  formed  by  lymph  cells 
which  accumulate  notably  around  the  blood  vessels  (perivas- 
cular) and  the  nerve  cells  (pericellular)  as  well.  The  lesions, 
when  present,  are  observed  most  frequently  in  the  motor  cen- 
ters of  the  oblongata  and  spinal  cord. 

The  following  observations  were  made  b}-  Babes,  in  1887  : 

I.  "In  animals  dead  from  street  rabies  there  are  found 
usually  a  hyperaemia  and  an  acute  generalized  cedema  of  the 
cerebral  meninges,  acute  hemorrhages  localized  around  certain 


MORBID    ANATOMY  317 

vessels,  as  well  as  inflammatory  lesions.  On  microscopic  ex- 
amination we  find  an  increase  of  the  plasma  cells,  augmenta- 
tion of  the  reticular  substance,  fibrinous  in  character,  between 
the  several  layers  of  the  meninges. 

2.  The  epithelium  of  the  cerebro-spinal  central  canal  has 
proliferated.  In  the  gray  matter  which  surrounds  the  canal, 
and  especially  in  that  of  the  floor,  hemorrhages,  sometimes 
symmetrical,  are  often  found.  Microscopically,  we  often  find 
an  obliteration  or  thrombosis  of  a  vessel  by  a  reticulated,  hya- 
line, pigmented  material  or  bj'  leucocytes  or  hyaline  globules, 
and  sometimes  a  hyaline  degeneration  or  even  inflammation  of 
the  vascular  tunic.  The  extravasated  blood  also  contains 
much  of  the  hyaline  material.  The  hemorrhages  are  often 
limited  b}'  the  lymphatic  sheath  of  the  vessels.  At  the  same 
time  the  epithelium  of  the  ventricles  and  central  canal  may  be 
partially  lost.  This  last  is  occasionally  filled  with  blood  or 
plugs,  either  granular  or  hyaline  in  character. 

3.  With  the  naked  eye  small  centers  of  degeneration 
may  sometimes  be  noted  in  the  gra}^  matter,  but  often  the}- 
may  be  sought  for  in  vain. 

4.  The  most  constant  lesions  are  microscopic  in  charac- 
ter ;  they  are  found  more  especially  in  tli£  gray  matter  sur- 
rounding the  cerebro-spinal  canal  and  in  the  motor  centers  of 
the  medulla  and  spinal  cord.  These  lesions  consist  at  first  in 
hypersemia  and  accumulations  of  embryonic  cells  around  the 
small  vessels,  perithelial  or  migrator}'  in  origin,  often  showing 
indirect  division  ;  finally  there  are  also  found  lesions  of  nerve 
cells. 

5.  The  lesion  of  the  nervous  elements  of  the  parts  indi- 
cated is  quite  characteristic  ;  it  consists  of  signs  of  prolifera- 
tion, namely,  in  the  presence  of  several  small  cells  in  place  of 
one  large  one,  or  in  a  uniform  degeneration  and  often  in  the 
appearance  of  vacuoles  with  a  reduction  in  size  or  disappear- 
ance of  the  nucleus,  or,  again,  its  chromatic  network  disap- 
pears. These  cells  frequenth'  contain  pigment.  Round  uni- 
nuclear, more  rarely  multinuclear,  elements  of  a  lymphatic 
origin  often  invade  the  protoplasm  even  of  the  cell  and  fill  out 


3l8  RABIES 

the  dilated  pericellular  lymphatic  spaces  by  a  multiplication  of 
small  nuclei. 

6.  The  lesion  of  medullary  substance  is  less  pronounced, 
it  consists  chiefly  of  an  oedema  of  the  medullary  sheath  of  the 
nerve  fibers. 

7.  In  certain  plasma  cells,  in  the  interior  of  and  around 
vessels,  sometimes  in  leucocytes,  in  lymphatic  spaces,  in  the 
altered  parts  of  certain  nerve  cells,  and  in  the  dilated  sheath 
of  nerve  fibers  may  be  seen  round  or  amoeboid  granules  about 
in  in  diameter,  pigmented  or  stainable  bj'  aniline  dyes,  and 
which  in  part  seem  to  posses  the  power  of  movement. 

More  recently  Babes  has  noted,  besides  the  lesions  above 
mentioned,  that  the  alteration  of  the  nerve  cell  is  usually 
accompanied  by  a  modification  of  their  protoplasmic  network 
and  concludes  that  "Whilst  admitting  that  the  lesions  of  rabies 
are  not  absolutel3^  characteristic,  and  that  it  may  be  that  in  a 
case  ot  diffuse,  very  acute  myelitis  similar  lesions  may  be 
found,  it  is  necessary  all  the  same  to  state,  that  neither  in 
writing  nor  in  my  personal  experience  have  I  ever  met  with  a 
similar  case,  so  that  at  present  we  may  consider  the  lesion  of 
rabies  as  characteristic.  In  other  infectious  diseases  there 
have  also  been  found  histological  lesions  characteristic  as  a 
whole,  although  composed  of  elements  not  absolutely  specific." 

Golgi  draws  attention  to  the  followingmorbid  changes  in 
rabies  : 

(i)  Changes  in  the  structure  of  the  nucleus,  all  the  vari- 
ous phases  of  karyokinesis  may  be  simulated,  yet  no  true 
nuclear  division  may  take  place.  (2)  Changes  in  the  body  of 
the  cells,  such  as  vacuole  formation,  bladder-like  transforma- 
tion of  the  cells.  Changes  may  also  be  recognized  by  methods 
directed  to  the  study  of  the  outer  form  of  the  cell.  Here 
varicose  appearances  of  the  cell  processes  may  be  seen. 
Granular  fatty  changes  ma}'  also  be  present.  An  important 
change  lies  in  the  displacement  of  the  nucleus.  The  periphery 
of  the  cell  becomes  homogeneous.  Granular  fatty  changes 
are  also  seen  in  the  neuroglia  cells.  (3)  Changes  in  the  inter- 
vertebral ganglia.  The  author  would  look  upon  these  ana- 
tomico-pathological changes  found  by  him  as  characteristic, 


MORBID    ANATOMY  3I9 

while  here  not  only  the  sum  total  of  the  changes,  bnt  also 
their  order  of  occurrence  and  mutual  interdependence  are  taken 
into  consideration. 

The  morbid  process  is  a  parenchj^matous  encephalo-mj-el- 
itis,  of  which  the  exact  exciting  case  is  as  yet  unknown. 
The  changes  are  thus  grouped  :  (i)  appearance  of  nuclear 
chromatin,  peculiar  cell  division  (neuroglia  cells  and  vascular 
endothelium,)  nuclear  movements  also  in  nerve  cells,  diffuse 
vascular  distension  and  leucocyte  infiltration,  re\ealing  a  con- 
dition of  irritation  ;  (2)  swelling,  vacuolation,  changes  of 
form,  granular  appearance  of  nerve  cells  and  neuroglia  ;  and 
(3)  more  advanced  changes  in  the  nerve  elements.  The 
changes  in  the  first  group  may  be  seen  as  earh-  as  five  days 
after  inoculation. 

In  a  more  recent  article  by  Germano  and  Capobianco 
attention  is  called  to  the  fact  that  the  destruction  of  some  of 
the  nerve  cells  in  rabid  animals  is  not  accepted  by  everybody, 
but  that  in  their  researches  they  have  been  able  to  confirm  the 
statements  made  bj^  Golgi,  that  instances  of  the  complete  dis- 
appearance of  nerve  cells  have  been  observed,  while  other  cells 
showing  fatty  degeneration  and  partial  destruction  of  their 
entirety  represent  intermediate  stages  between  the  normal  cell 
and  its  total  disappearance.  The  alteration  of  the  nucleus 
may  precede  or  follow  that  of  the  cell  bod\'. 

The  nerve  fibers,  either  in  the  white  or  gray  matter, 
undergo  a  certain  amount  of  change.  In  a  longitudinal  sec- 
tion of  the  my  el,  especially  through  the  ventro-lateral  columns, 
there  are  noted  marked  changes  in  the  axis  cylinders.  In 
some  cases  they  appear  uniformly  swollen  for  their  whole 
length,  while  in  others  there  are  varicose  enlargements.  In 
the  swollen  portions  there  were  frequently  observed  small 
vacuoles  which  interrupted  the  continuity  of  the  axis  cylinder. 

During  the  year  1900,  the  discovery  of  changes  distinctive 
of  rabies  was  announced  by  Van  Gehucten  and  Nelis.  These 
changes  are  found  in  the  peripheral  ganglia  of  the  cerebro 
spinal  and  sympathetic  systems  and  are  especially  marked  in 
the  plexiform  ganglion  of  the  pneumogastric  nerve  and  the 
gasserian  ganglion.      Normally  these  ganglia  are  composed  of 


320  RABIES 

a  supporting  tissue  holding  in  its  meshes  the  nerve  cells,  each 
one  of  which  is  enclosed  in  a  capsule,  made  up  of  a  single 
la5'er  of  endothelial  cells.  The  action  of  the  rabic  virus  seems 
to  exercise  its  effect  on  these  cells  particularly,  bringing  about 
an  abundant  multiplication  of  the  cells  forming  this  capsule, 
leading  finalh'  to  the  complete  destruction  of  the  normal 
ganglion  cell  and  leaving  in  its  place  a  collection  of  round 
cells.  Ordinarily  a  considerable  number  of  ganglion  cells  will 
be  found  which  have  undergone  only  a  slight  change,  but 
under  certain  conditions  the  process  is  so  widespread  that  all 
the  ganglia  cells  are  destroyed.  The  intensitj^  of  these  changes 
varies  in  different  animals  ;  the}'  are  perhaps  most  pronounced 
in  the  dog,  less  marked  in  man  and  still  less  in  the  rabbit. 

Much  of  the  value  of  these  findings  consists  in  their  mak- 
ing a  sure  and  quick  means  of  diagnosis.  It  is  possible  to  com- 
plete the  examination  within  six  hours  after  the  death  of  the 
animal,  and  under  ordinary  circumstances  a  positive  opinion 
can  be  given  in  from  24  to  36  hours.  It  is  important  that  the 
animal  should  be  allowed  to  die  and  not  be  killed  prematurely, 
as  where  the  disease  is  not  permitted  to  run  its  full  course  end- 
ing in  death,  the  changes  may  be  absent  or  only  slightly 
developed. 

§242.  DifTerential  diagnosis.  From  the  often  obscure 
manner  of  infection,  the  long  period  of  incubation,  the  vari- 
able symptoms  and  the  absence  of  gross  morbid  changes  char- 
acteristic of  the  disease,  it  is  easy  to  mistake  rabies  for  various 
other  nervous  disorders  and  vice  versa,  unless  a  definite  method 
of  diagnosis  can  be  availed  of. 

Diagnosis  by  animal  inoculation.  The  method  which  the 
experience  of  pathologists  has  shown  to  be  the  best,  is  the  sub- 
dural inoculation  of  rabbits  with  a  suspension  of  the  brain  or 
spinal  cord  of  the  suspected  animal.  The  subdural  inoculation 
with  the  brain  tissue  of  rabid  animals  was  first  demonstrated 
by  Pasteur  to  be  more  reliable  and  more  rapid  in  its  results 
than  the  subcutaneous  injections.  The  procedure  is  simple. 
The  brain  of  the  suspected  animal  is  removed  with  aseptic 
precautions  as  soon  as  possible  after  death.  A  small  piece  of 
the  brain  or  spinal  cord  is  placed  in  a  sterile  mortar  and  thor- 


RABIES  321 

oughly  ground  with  a  few  cubic  centimeters  of  sterile  water 
or  bouillon.     This  forms  the  suspension  to  be  injected. 

The  hands  of  the  operator  and  all  instruments  are  care- 
fully disinfected.  The  rabbit  is  etherized,  the  hair  clipped 
from  the  head  between  the  eyes  and  ears,  and  the  skin 
thoroughly  washed  and  disinfected.  A  longitudinal  incision 
is  then  made,  the  skin  and  subcutaneous  tissue  held  back  by 
means  of  a  speculum,  a  crucial  incision  is  made  in  the  perios- 
teum on  one  side  of  the  median  line,  to  avoid  hemorrhage  from 
the  longitudinal  sinus,  and  the  four  parts  of  the  periosteum 
reflected  or  pushed  back.  By  the  aid  of  a  trephine  a  small- 
button  of  bone  is  easilj'  removed  leaving  the  dura  mater  ex- 
posed. With  a  hypodermic  syringe  a  drop  or  more  of  the 
rabid  brain  suspension  is  injected  beneath  the  dura,  the  perios- 
teum is  replaced,  the  skin  carefully  sutured  and  disinfected 
and  the  rabbit  returned  to  its  cage.  As  soon  as  the  influence 
of  the  anaesthetic*  has  passed  off  the  rabbit  shows  no  appear- 
ance of  discomfort.  If  the  operation  is  performed  in  the  fore- 
noon the  animal  partakes  of  its  evening  meal  with  the  usual 
relish.  The  inoculation  wound  heals  rapidly  and  the  rabbit 
exhibits  every  appearance  of  being  in  perfect  health  until  the 
beginning  of  the  specific  symptoms,  which  occur  ordinarily  in 
from  fifteen  to  thirty  days  after  the  inoculation.  Occasionally 
the  symptoms  appear  earlier  than  fifteen  days  and  in  some 
cases  the  rabbits  are  not  attacked  for  from  one  to  three 
months. 

Sy))iploi)is.  The  symptoms  following  the  inoculation  are 
quite  uniform.  There  is,  however,  a  marked  difference  in  the 
length  of  time  the  rabbits  live  after  the  initial  manifestation  of 
the  disease.  The  fact  should  be  clearly  stated  that  rabbits  do 
not  ordinarily  become  furious.  In  some  instances  they  are 
somewhat  nervous  for  a  day  or  two  preceding  the  paralysis. 
There  appears  to  be  marked  hypersesthesia.  Usually  the  first 
indication  of  the  disease  is  a  partial  paralysis  of  one  or  both 
hind  limbs.     This  gradually  advances  until  the  rabbit  is  com- 


■*Ether  should  be  used  in  preference  to  chloroform  for  rabbits,  as  the 
latter  frequently  causes  death,  while  the  former  can  be  administered 
with  comparative  safety. 


322  RABIES 

pletely  prostrated,  the  only  evidence  of  life  being  a  slight  res- 
piratory movement.  The  head  occupies  different  positions. 
In  some  it  is  drawn  backward  as  in  tetanus  ;  in  others  it  is 
drawn  down  with  the  nose  near  the  fore  legs  and  in  still 
others  it  is  extended  as  if  the  animal  were  sleeping.  The 
period  of  this  complete  paralj'sis  varies  from  a  few  hours  to  a 
few  days,  but  ordinarily  it  has  not  exceeded  twenty-four 
hours.  Although  these  animals  are  unable  to  move  volun- 
tarih'  there  is  a  reflex  action  of  the  limbs  until  a  very  short 
time  before  death. 

During  the  period  of  incubation  the  temperature  of  the 
rabbits  is  normal.  As  the  time  approaches  for  the  first  symp- 
toms to  appear  there  is  an  elevation  of  temperature  of  from  i 
to  2  degrees,  which  continues  for  a  variable  length  of  time, 
but  rarely  longer  than  two  days.  This  is  followed  by  a  grad- 
ual or  usually  a  more  rapid  drop  to  the  subnormal,  which  con- 
tinues to  the  end. 

The  differential  diagnosis  in  experimental  animals  is  not 
difficult.  Rabbits  inoculated  with  several  varieties  of  patho- 
genic bacteria  frequently  exhibit  symptoms  of  paralysis  for  a 
brief  period  preceding  death.  In  cases  oi  injury  to  the  brain 
or  spinal  cord  there  may  also  be  parah^sis,  which  in  the 
absence  of  the  history  of  the  case  might  be  taken  for  that  of 
rabies.  In  these  cases,  however,  the  symptoms  appear  very 
soon  after  inoculation.  This  is  especially  true  when  the  par- 
alysis is  due  to  mechanical  injurj^  of  the  brain  or  to  irritation  or 
septic  substances  and  in  the  case  of  the  pathogenic  bacteria  if 
paralysis  occurs  at  all  it  is  almost  invariably  preceded  by 
marked  disability.  This  method  of  diagnosing  rabies  requires 
that  the  inoculated  animals  remain  apparently  well  for  a  con- 
siderable length  of  time  after  the  subdural  inoculation  and 
before  the  paralytic  symptoms  appear. 

The  lesions  found  on  the  post-mortem  examination  are 
also  of  much  assistance  in  making  a  diagnosis.  If  the  animal 
died  from  septicaemia  or  brain  injur}'  there  will  be  lesions 
almost  invariably  recognizable  in  the  brain  or  viscera.  In  the 
case  of  septicaemia  a  bacteriological  examination  will  reveal 
the  presence  of  microorganisms.      If  the  death  was  caused  by 


DIAGNOSIS  323 

rabies  the  inoculation  wound  in  the  head  should  be  healed 
perfectly,  there  should  be  no  abscess  and  the  meninges  should 
be  free  from  exudates  and  the  brain  itself  should  appear  per- 
fectly normal,  except  that  in  rare  cases  there  may  be  a  slight 
injection  of  the  blood  vessels.  The  viscera  are  ordinarily 
normal  in  appearance,  with  possibly  the  exception  of  the  liver, 
which  we  have  frequently  found  to  be  deeply  reddened  and 
the  gastric  mucosa,  which  not  infrequently  shows  dark  patches, 
indications  of  disintegrated  hemorrhagic  areas.  A  bacterio- 
logical examination  fails  to  reveal  the  presence  of  micro- 
organisms in  either  the  tissues  01  blood.  Another  important 
point  which  has  been  noticed  is  an  intense  rigor  mortis  follow- 
ing death  from  rabies.  Kinyoun  states  that  this  was  a  con- 
stant feature  of  this  disease  in  all  of  the  produced  cases  which 
have  come  under  his  observation.  Wesbrook  has  not  found 
this  condition. 

Animals  other  than  rabbits  have  been  used  and  a  number 
of  other  methods  of  inoculation  have  been  proposed. 

Diag)iosis  by  histological  examiiiation.  The  rapid  diagnosis 
by  means  of  the  histological  changes  pointed  out  by  Van 
Gehucten  and  Nelis  has  been  very  successful  in  the  experience 
of  Ravenel.  He  states  that  :  "The  ganglion  of  the  pneumo- 
gastric  nerve  is  selected  by  preference  and  should  be  removed 
as  soon  as  possible  after  the  death  of  the  animal.  It  is  put 
into  absolute  alcohol  or  ten  per  cent  formalin  solution.  If  put 
into  absolute  alcohol  it  should  be  removed  to  a  fresh  portion 
of  alcohol  at  the  end  of  six  hours,  in  which  it  rem.ains  for  six 
hours,  when  it  may  be  transferred  for  one  hour  to  a  mixture  of 
absolute  alcohol  and  chloroform,  and  then  put  for  one  hour  in 
pure  chloroform,  then  for  one  hour  in  a  mixture  of  chloroform 
and  paraffin,  and  lastly  imbedded  in  paraffin.  If  formalin  is 
used  for  fixing,  the  ganglion  should  be  removed  at  the  end  of 
six  or  eight  hours,  put  for  six  hours  more  in  95  per  cent 
alcohol  and  then  into  absolute  alcohol  for  six  hours,  after 
which  it  ma}'  be  fixed  in  blocks  for  cutting,  by  mucilage  or 
gum  arable,  or  else  imbedded  in  collodion.  The  characteristic 
■changes  of  the  capsule  are  brought  about  best  by  the  use  of 
Jiematoxylin,  or  hemalum  and  eosin.     The  method  of  Nissl 


324  RABIES 

gives  good  results  also  but  as  it  requires  some  special  technical 
knowledge  to  be  efficiently  carried  out  the  former  is  recom- 
mended for  its  simplicity  and  ease  of  execution.  This  method 
has  stood  the  test  in  Europe  and  America  for  nearly  two  years 
and  although  a  large  number  of  animals  having  different 
diseases  have  been  examined  with  the  object  of  determining 
whether  or  not  these  changes  may  occur  in  other  conditions, 
they  have  never  been  found. 

At  the  laboratory  of  the  State  I^ive  Stock  Sanitary  Board, 
which  was  the  first  in  this  country  to  take  up  this  method, 
fifty-two  cases  have  been  examined  since  May,  1900,  without 
a  single  failure.  These  cases  have  occurred  in  mankind,  dogs, 
cov/s,  cats  and  rabbits,  and  the  characteristic  changes  have 
been  found  in  each  of  these  species.  We  have  not  had  an 
opportunity  of  examining  horses,  sheep  or  swine.  In  this 
laboratory  it  has  replaced  the  slow^er  and  less  certain  method 
of  inoculation  almost  entirely.  Inoculations  are  now  practiced 
only  in  those  cases  in  which  the  material  is  sent  in  such  condi- 
tion that  the  microscopic  examination  is  impossible." 

§  243.  Prevention  and  treatment.  The  prevention  of 
rabies  infection  resolves  itself  into  two  procedures.  (1)  The 
destruction  of  all  ownerless  and  vagrant  dogs  and  (2)  the 
muzzling  of  all  dogs  that  appear  upon  the  streets  or  in  public 
places.  In  thus  preventing  the  propagation  of  the  virus 
as  shown  by  the  results  obtained  in  Germany  and  Great 
Britain  the  disease  will  be  practically  exterminated. 

There  is  no  treatment  for  rabies  except  the  preventive 
inoculation  known  as  the  Pasteur  treatment  by  which  an  im- 
munity is  produced  by  the  subcutaneous  injection  of  the  virus 
of  rabies  in  an  attenuated  form ,  beginning  with  the  mildest  virus 
and  going  gradually  up  to  one  which  possesses  nearly  or  full 
virulence.  The  attenuation  of  the  virus  is  brought  about  by 
drying  at  a  fixed  temperature  and  the  action  of  the  atmosphere. 
Depending  upon  the  length  of  time  the  virus  is  exposed  to  the 
influences,  we  can  obtain  any  degree  of  virulence  desired,  the 
loss  of  virulence  under  fixed  conditions  being  quite  uniform. 

The  disease  as  seen  in  dogs  infected  naturally  was  called 
by  Pasteur  "street  rabies"  and  the  virus  of  such  animals  is. 


DIPHTHERIA    IN    FOWLS  325 

known  as  the  "virus  of  street  rabies."  Such  virus  will  as  a 
rule  produce  the  disease  in  rabbits  by  intra-crauial  inoculation 
in  from  three  to  four  weeks.  By  inoculating  rabbits  in  series 
one  from  the  other,  a  reduction  of  the  period  of  incubation  is 
obtained.  After  about  100  passages  rabbits  will  die  with  cer- 
tainty and  great  regularity  on  the  sixth  or  seventh  day  after 
inoculation.  Beyond  this  point  no  increase  of  virulence  has 
been  obtained.      This  is  the  fixed  virus  of  Pasteur. 

REFERENCES. 

1.  Babes.  Sur  certains  caracteres  des  lesions  histologiques  de  la 
rage.     Ann.  de  V InstihU  Pasteur.     Vol.  VI.     209-223. 

2.  Cabot.  Report  on  experimental  work  on  the  dilution  method 
of  immunization  from  rabies.  Jour.  Experimental  Med.    Vol.  IV.    1899. 

3.  Dulles.  Disorders  mistaken  for  hydrophobia.  Trans,  of  the 
Med.  Soc  of  the  State  of  Fen  n.      18S4. 

4.  Fleming.     Rabies  and  hydrophobia. 

5.  KeirlE.  a  report  on  the  autopsies  on  four  recent  cases  of 
rabies  and  a  bacteriological  examination  of  a  rabid  dog,  together  with 
the  recent  laboratory  experiments.  Maryland  3Ied  Jour.  Vol.  XXXVIII. 

No.  I.      1897. 

6.  Law  Rabies.  A  System  of  Practical  Medicine  by  American 
Authors.     Vol.  III.      1898. 

7.  M.\cClure.  Rabies-hydrophobia.  Supplement  to  the  Annual 
Report  of  the  Michigan  Board  of  Health.     1895. 

8.  Moore  and  Fish.  .\  report  on  rabies  in  Washington,  D.  C. 
Annual  Report,  U.  S.  Bureau  of  Animal  Industry.     1895-6. 

9.  Public  Health  Commission,  District  of  Columbia.  Rabies. 
Bui.  2j.      U.  S.  Bureau  of  Animal  Industty.     1900 

10.  R.WENEL  AND  McCarthy.  The  rapid  diagnosis  of  rabies. 
Univ.  of  Penn.  Med.  Magazine.     January.     1901. 

11.  Ravenel.     Rabies    Bul.jg.  Dept.  of  Agr.,  State  of  Penn.   1901. 

12.  S.^LMON.  Rabies,  its  cause,  frequency  and  treatment.  Year 
Book,  Dept.  of  Agriculture.      Washington,  D.  C.     1900. 

13.  Salmon.  Rabies  in  the  District  of  Columbia.  Circular  30, 
U.  S.  Bureau  of  Animal  Industry.     1900. 

14.  SuzoR.   Hydrophobia.   An  account  of  M.  Pasteur's  system.    1887. 

15.  Wesbrooic.  Preliminary  report  on  the  laboratory  diagnosis  in 
twenty  cases  of  suspected  rabies.       Trans.  Am.   Public  Health   Assn. 

898. 


DIPHTHERIA  IX  FOWLS. 


§  244,  Characterization.  Diphtheria  of  birds  is  an  in- 
fectious disease  the  lesions  of  which  first  appear  on  the  mucous 
membrane  of  the  nasal  passages,  the  eyes,  the  mouth,  the 
pharynx  and  larynx  and  which  may  extend  to  the  trachea, 
bronchi,    the    air-sacs,    the    intestines  and   possibly    to    other 


326  DIPHTHERIA    IN    FOWLS 

abdominal  organs.  The  disease  is  determined  b}-  a  grayish- 
yellow,  fibrinous  exudate  which  forms  upon  the  mucous  surface 
of  the  parts  mentioned.  The  exudate  may  be  so  abundant  as 
to  obstruct  the  air  passages.  In  some  outbreaks,  it  is  very 
acute,  progresses  with  great  rapidity  and  destroys  most  of  the 
birds  attacked.      It  is  popularly  known  as  "roup.  "§ 

Fowls  (genus  Gallus)  and  pigeons  (genus  Coluviba)  are 
most  commonly  attacked  and  the}-  are  the  only  ones  considered 
in  this  discussion.  Avian  diphtheria  is  reported,  however,  to 
attack  turkeys,  ducks,  pea-fowls,  pigeons  and  pheasants.  It 
is  presumed  that  wild  birds  may  be  afifected. 

Avian  diphtheria  is  quite  distinct  from  human  diphtheria. 
There  are  cases  on  record,  however,  which  indicate  that  the 
diphtheria  of  fowls  may  be  communicated  to  children  and 
cause  a  serious  and  even  fatal  sore  throat.  On  the  other  hand, 
it  is  asserted  that  diphtheria  of  children  is  sometimes  com- 
municated to  fowls  and  that  the  virus  may  be  thus  preserved 
for  a  considerable  time  and  again  be  transmitted  to  children. 
Concerning  this  point  additional  investigations  are  needed. 

§245.  History.  The  history  of  this  disease  is  somewhat 
obscure.  It  is  evident  from  the  literature,  that  fowls  have 
always  been  subject  to  various  affections  of  the  head  but  the  first 
investigation  of  this  class  of  maladies  seems  to  have  been  made 
by  Loeffler-'^  in  1884.  Since  that  time  Klemmer,t  Babes  and 
Puscarin,!  Eberlin,||  L,oir  and  Ducloux*  and  others  have  stud- 
ied diseases  known  as  diphtheria  in  pigeons,  fowls  and  other 
birds.  The  disease  was  investigated  by  the  Bureau  of  Animal 
Industry  in  1893-4. 

§  246.  Etiology.  In  1884,  Loeffler  discovered  a  bac- 
terium which  he  believed  to  be  the  specific  cause  of  diphtheria 
in   fowls   and  with  which   he   could   produce   the  disease.     It 

§The  origin  of  this  term  is  somewhat  obscure,  but  it  is  supposed  to 
be  a  corruption  of  croup,  and  its  application  explained  on  account  of  a 
peculiar  hoarseness  accompanying  the  respiration  of  the  affected  birds. 

^Mitt.  aus  dem  Kaiserlichen  Gesundheitsanite.   Bd.  II.   (1SS4),  S.  214. 

tBerliner  thieriirzt.  Wochenschrift.    1890,  No.  18,  S.  13S. 

jZeitschrift  f.  Hygiene.     Bd  VIII.   (1890),  S.  374. 

IIMonatshefte  f.  Thierheilkunde.    Bd.  V.    (1894),  S.  433. 

*|Ann.  de  rinst.  Pasteur.    Tome  VIII.   (1S94),  p.  599. 


SYMPTOMS  327 

differed  from  the  diphtheria  bacterium  in  man.  Loir  and 
Ducloux  isolated  a  still  different  organism.  The  writer  found 
in  the  exudates  of  the  earlier  stages  of  the  disease  a  bacterium 
belonging  to  the  septicaemia  hemorrhagica  group.  It  was 
rapidly  fatal  to  rabbits  but  the  diphtheretic  lesions  could  not 
be  produced  by  inoculation  in  fowls.  There  are  marked  differ- 
ences in  the  different  bacteria  isolated  and  suspected  of  etio- 
logical significance.  It  is  not  positive,  however  that  the  same 
disease  was  studied  by  the  different  writers.  There  is  little  doubt 
of  the  specific  nature  of  the  disease.  It  is  usually  introduced 
into  a  flock  by  the  exposure  of  the  birds  to  sick  ones  at  shows 
or  by  bringing  affected  birds  on  the  premises.  The  contagion 
may  be  carried  by  birds  which  have  the  disease  in  so  mild  a 
form  that  the\^  show  no  symptoms  of  it.  There  is  a  general 
belief  that  the  disease  may  be  developed  b}-  exposure  of  birds 
to  draughts  of  air  or  by  keeping  them  in  damp,  filthy  and 
badly-ventilated  houses.  It  is  presumable  that  this  belief  in 
its  etiology  is  not  well  founded  because  of  confusion  existing 
concerning  the  earh'  symptoms  of  acute  diphtheria  and  those 
of  all  stages  of  the  clironic  form  and  those  of  simple  colds  and 
catarrhs.  Dampness  and  lack  of  ventilation  no  doubt  favor 
the  maintenance  of  the  virus  when  introduced  and  predispose 
the  birds  to  the  disease.  The  specific  cause  of  the  disease 
known  as  diphtheria  or  roup  in  chickens  and  pigeons  in  the 
opinion  of  the  writer  is  not  known. 

i^  247.  Symptoms.  There  is  a  watery  secretion  from 
the  nostrils  and  often  from  the  eyes,  with  general  weakness 
and  prostration  greater  than  would  be  expected  from  simple 
catarrh.  The  birds  sit  with  the  back  arched,  the  head  and 
neck  drawn  down  towards  the  body,  the  plumage  roughened  ; 
the  respiration  is  more  or  less  obstructed,  rapid  and  audible, 
the  vision  is  impaired  and  swallowing  is  difficult.  There  is 
frequent  shaking  of  the  head,  sneezing  and  expectoration  of 
mucous  secretions.  If  the  mouth  is  examined  at  this  early 
period  the  tongue  is  found  to  be  pale,  while  .small  grayish 
spots,  shaded  wath  black  and  slightly  projecting  above  the 
surface  are  seen  along  the  border,  the  upper  surface  or  at 
the  base. 


328  DIPHTHERIA    IN    FOWLS 

The  following  day  the  condition  is  aggravated,  the  tem- 
perature is  several  degrees  above  normal,  the  appetite  has  dis- 
appeared and  there  is  diarrhoea  with  greenish  or  yellowish 
evacuations.  From  the  open  beak  there  escapes  a  thick, 
stringy,  grayish  mucus.  The  eyes  are  unnaturally  dilated, 
projecting  and  possibly  partly  covered  with  the  thick  secretion 
which  has  accumulated  between  the  lids.  The  nostrils  are 
obstructed  by  the  thickened  and  dried  secretion.  Walking  is 
irregular  and  difficult.  The  mucous  membrane  of  the  mouth 
and  pharynx  is  congested  and  shows  numerous  dark  red  eleva- 
tions covered  with  fibrinous  exudate.  The  patches  on  the 
tongue  have  increased  in  size,  they  are  gray  in  color,  dried 
along  the  edges  of  the  tongue  but  soft  and  flattened  upon  its 
upper  surface.  They  are  covered  with  membranous  deposits. 
The  voice  often  fails. 

^  248.  Morbid  anatomy.  The  lesions  are  largely  local- 
ized on  the  mucosa  of  the  head.  With  the  exception  of  emacia- 
tion, there  are  no  lesions  or  evidence  of  organic  disease.  The 
cause  of  death  and  the  extreme  emaciation  is  difficult  to  explain 
in  those  cases  where  the  lesions  were  confined  to  one  eye  or  to 
the  mucosa  of  the  nares,  excepting  on  the  supposition  that  some 
poisonous  or  toxic  substance  was  absorbed  from  the  seat  of  the 
disease.  In  those  cases  where  the  lesions  are  in  both  eyes, 
or  in  the  mouth  and  throat,  difficulty  in  finding  or  swallowing 
food  affords  a  rational  explanation. 

In  some  cases  the  exudate  is  of  a  croupous  character,  in 
others  of  a  diphtheritic  nature.  Three  stages  or  varieties 
of  lesions  which  represent  the  types  of  this  disease  as  encount- 
ered in  this  country  may  be  more  definitely  defined  as  follows. 
(i)  An  exudate  of  a  serous  or  muco-purulent  character 
in  the  conjunctiva  and  nasal  cavities.  Ordinarily  this  condition 
cannot  be  recognized  in  the  mouth.  The  mucosa  in  these 
cases  are  apparently  but  slightly  altered. 

(2)  The  mucosa  over  a  small  or  larger  area  is  covered 
with  a  spreading  exudate  of  a  grayi.sh  or  yellow  color.  It  is 
firmly  attached  to  the  mucous  membrane  and  when  removed 
leaves  a  raw,  bleeding  surface.  Sections  through  this  exudate 
and  the  subjacent  tissues  show  that  the  epithelial  layer  is  des- 


Plate  VIII 


:-*>i^l' 


,'      O  V  TV 


-:C:-}:k''i:^^2^''^*^'?^f???? 


•^-f*^^^^ 


^^  x:r-:'i^^ 


N 


-    5    T,^     .^      *. 


I. 


,--rt»!^*J>'.»,^        ,^ip«!^r",E 


2. 


/r 


DIPHTHERIA  IN   PIGEONS. 


MORBID    ANATOMY  329 

troyed  and  the  underlying  tissue  infiltrated  with  cells.      The 
extent  of  the  infiltration  varies  in  different  individuals. 

(3)  The  mucosa  is  covered  with  a  thick  mass  of  exu- 
date, varying  in  color  from  a  milky  white  to  a  lemon  yellow 
or  brown.  It  is  easily  removed,  leaving  a  more  or  less  granu- 
lar and  healed  surface.  This  sloughed  mass  is  frequently 
dried  at  its  margins  to  the  adjacent  tissue.  It  emits  a  strong 
putrid  odor,  due  to  decomposition.  The  drying  of  the  mar- 
gins prevents  the  fowl  from  expelling  the  exudate  after  it  be- 
comes separated  from  the  underlying  tissue. 

The  evidence  to  support  the  supposition  that  the  three 
forms  or  types  of  exudate  described  are  different  stages  in  the 
same  morbid  process,  as  gathered  from  the  post-mortem  notes 
and  bacteriological  study  of  the  cases  investigated,  ma)'  be 
summarized  as  follows. 

(a)  Abnormal  conditions,  representing  the  intermediate 
and  connecting  links  between  the  types  of  lesions,  are  fre- 
quently encountered. 

(d)  Although  at  the  time  of  examination  (post-mortem) 
but  one  form  of  exudate  is  usually  present  in  a  single  fowl,  there 
are  exceptions,  in  which  two  and  occasionally  the  three  forms 
are  coincident.  Thus  the  eye  is  covered  with  a  sloughed 
exudate,  the  posterior  nares  contains  a  layer  of  muco-purulent 
substance  and  on  the  muco.sa  of  the  mouth  are  areas  of  a 
diphtheritic  exudate. 

In  fowls  which  die,  the  exudates  are  for  the  greater  part 
in  the  advanced  stage,  although  fatal  cases  occur  in  which  the 
lesions  are  restricted  to  an  abnormal  quantity  of  a  serous  or 
muco-purulent,  more  or  less  viscid,  exudate  in  the  conjunctiva 
or  nasal  cavities.  The  best  illustration  of  the  diphtheretic 
process  is  found  in  fowls  killed  for  examination  in  the  second 
stage  of  the  disease.  The  distribution  of  the  lesions  shows 
that  the  conjunctiva  is  most  frequently  affected.  The  exudate 
in  the  nasal  cavities  is  in  some  cases  undoubtedly  the  result  of 
the  coagulation  of  the  liquid  which  has  passed  during  the  course 
of  the  first  stage  from  the  conjunctiva  through  the  lachrymal 
duct  into  the  nares.  In  certain  cases,  however,  the  lesions  appear 
in  the  nares  primarily.   Sections  of  the  exudate,  with  subjacent 


330  DIPHTHERIA    IN    FOWLS 

tissue  from  the  cornea  and  the  mouth,  show  that  there  is  a  cell 
infiltration  into  the  mucosa  which  destroys  the  epithelial  layer 
and  frequently  the  submucous  tissues  to  a  considerable  depth. 
See  Plate  YIU. 

The  fact  should  not  be  overlooked  that  the  disease  in  the 
eye  is  usually  confined  to  the  conjunctiva  and  the  cornea,  the 
posterior  portion  remaining  apparently  normal. 

From  the  observations  thus  far  made  the  provisional 
theory  is  entertained  that  the  three  forms  of  the  exudate — 
serous  or  muco-purulent,  diphtheritic  and  sloughed  mass — 
represent  three  stages  in  the  course  of  the  same  disease.  It  is 
easily  understood  that  fowls  examined  in  the  first  stage  would 
be  said  to  be  affected  with  a  catarrhal  condition  of  the  mucosa 
of  the  eyes  or  nares.  It  is  liighly  probable  that  in  many  cases 
the  disease  never  reaches  the  second  stage  and  if  these  cases 
alone  were  examined  the  diphtheritic  condition  would  not  be 
suspected.  It  appears,  however,  that  in  the  majority  of  cases 
the  disease  runs  its  course  and  membranes  are  formed,  slough 
and  recovery  follows.  It  is  further  presumable  that  the  disease 
in  question  appears  sometimes  in  a  virulent  and  destructive 
form.  I  am  in  possession  of  statements  from  poultry  raisers 
which  show  that  there  are  occasional!}'  epizootics  of  a  disease 
characterized  bj-  exudates  in  the  eyes,  nose  or  mouth,  which 
runs  a  rapidly  fatal  course.  It  appears  that  it  is  such  out- 
breaks which  have  been  reported  in  Europe  as  diphtheria  and 
not  the  low  form  of  chronic  disease  which  has  been  studied  in 
this  country. 

§  249.  Relation  of  diphtheria  in  man  to  that  in  fowls. 
A  comparison  of  the  bacillus  of  diphtheria  in  man  (  Klebs- 
Loeffler)  with  those  described  from  diphtheria  in  fowls,  shows 
that  morphologically  and  in  their  pathogenesis  for  experi- 
mental animals  the  organisms  are  in  no  way  alike.  There  is 
also  a  marked  difference  in  the  nature  of  the  exudate  in  fowls 
and  in  man.  The  non-identity  of  these  diseases  has  been 
clearly  pointed  out  by  Menard*.  Although  these  maladies  are 
shown  by  several  observations  to  be  unlike  in  their  etiology 
and   the   character  of  their  lesions,   the  transmission   of  fowl 


*Revue  d'Hygiene.    Tome  XII.    ( iSgo),  p.  410. 


RELATION    TO    HUMAN    DIPHTHERIA  331 

diphtheria  to  the  human  species,  and  vice  versa,  is  affirmed  by 
several  vi^riters. 

Gerhardtf  reports  4  cases  of  diphtheria  in  Wesselhausen, 
Baden,  among  6  workmen  who  had  charge  of  several  thou- 
sand fowls,  many  of  which  died  of  diphtheria.  There  were 
no  other  cases  of  diphtheria  in  the  neighborhood  and  the  evi- 
dence was  quite  conclusive  that  the  disease  was  contracted 
from  the  affected  fowls.  It  is  also  stated  that  an  island  on  the 
northeastern  coast  of  Greece  had  been  free  from  diphtheria  for 
at  least  a  third  of  a  century,  when  a  dozen  turkeys,  several  of 
which  were  diseased,  were  introduced.  Soon  afterwards  diph- 
theria appeared  in  a  house  near  the  garden  where  the  turkeys 
were  kept.  The  disease  became  epidemic  on  the  island  caus- 
ing the  death  of  36  people,  over  40  per  cent  of  those  attacked. 

Debrie^:  reports  briefly  the  clinical  historj-  of  6  cases  of 
diphtheria  which  occurred  in  the  garrison  of  Sebdou,  and  states 
that  while  the  sixth  case  (2  were  fatal )  was  still  under  treat- 
ment in  the  hospital  10  fowls  kept  in  a  house  not  far  from  the 
hospital  were  attacked  with  diphtheria  and  exhibited  symp- 
toms strikingly  like  those  present  in  the  human  beings.  Five 
of  the  10  fowls  died  and  two  heads  were  sent  to  Arloing,  who 
confirmed  the  diagnosis  of  fowl  diphtheria.  The  fowls  were 
fed  by  a  hospital  attendant  and  it  was  ascertained  that  an 
identical  outbreak  had  occurred  among  the  fowls  at  a  neighbor- 
ing place  from  which  one  of  the  6  cases  of  human  diphtheria 
had  been  brought.  Debrie  is  inclined  to  the  view  that  human 
diphtheria  is  transmissible  to  fowls  and  fowl  diphtheria  to  man. 

Cole*  reports  a  case  near  Jacksonville,  111.,  where  a  flock  of 
fowls  became  affected  with  a  disease  characterized  b}'  an  exu- 
date on  the  mucosa  of  the  head.  Some  of  the  exudates  emit- 
ted a  foul  odor.  As  the  weather  was  cold,  one  of  the  chick- 
ens was  taken  into  the  house  where  a  child  about  2^2  5'ears 
old  fondled  it.  Four  days  later  the  child  was  taken  sick  ap- 
parently with  diphtheria,  from  which  it  died.  There  were  no 
other  cases  in  the  neighborhood  and  the  affected  chicken  was 
the  only  possible  source  of  infection. 


tRevne  f.  Thierheilkunde  u.  Viehzucht.    Bd.  VI.    (1S83),  p.  180. 
^Reviewed  in  Centralblatt  f.  Bakteriologie.    Bd  XIII.  (1893),  S.  730. 
*Archives  of  Pediatrics,  XI,  (1894),  p.  381. 


332  DIPHTHERIA    IN    FOWLS 

The  diphtheritic  disease  of  fowls  reported  by  Loir  and 
Ducloux  in  Tunis,  in  1894,  spread  to  the  people  of  that  place, 
resulting  in  an  epidemic  of  serious  proportions.  Menard 
refers  to  the  fact  that  men  emplo3ed  to  feed  young  squabs  con- 
tracted diphtheria  by  blowing  the  masticated  food  into  the 
mouth  and  crop  of  squabs  suffering  with  that  disease.  Schrev- 
ens|  reports  several  cases  of  diphtheria  in  children  in  which  he 
traces  the  source  of  infection  to  certain  poultry. 

Although  the  number  of  reported  cases  of  the  transmis- 
sion of  fowl  diphtheria  to  the  human  species  and  vice  versa,  is 
small  in  comparison  with  the  extent  of  the  disease  in  poultry, 
the  evidence  that  such  a  transmission  is  possible  is  quite  suffi- 
cient to  discourage  the  careless  handling  of  diseased  fowls.  It 
is  a  quite  common  practice,  especially  in  the  rural  districts,  to 
bring  the  sick  chickens  into  the  house  for  treatment,  where 
the  children  of  the  household  are  allowed  to  fondle  them  at 
will.  It  is  not  improbable  that  when  this  disease  is  thoroughly 
investigated  the  number  of  cases  of  direct  infection  from  this 
source  will  be  found  to  be  much  larger  than  it  is  at  present 
supposed.  Until  such  investigations  are  satisfactorily  com- 
pleted the  indiscriminate  handling  of  diphtheritic  chickens 
especially  by  children  and  the  exposure  of  fowls  to  the  infec- 
tion of  diphtheria  in  the  human  species,  whereby  they  may 
become  carriers  of  the  virus,  should  be  strenuously  avoided. 

§  250.  Prevention  In  order  to  prevent  this  disease  it 
is  evident  that  many  conditions  must  be  strictly  complied 
with.  The  character  of  the  food  and  the  general  sanitary  con- 
ditions, including  cleanliness,  ventilation  and  the  temperature 
of  the  poultry  houses  must  be  considered.  Undoubtedly 
there  is  much  to  be  learned  in  connection  with  the  proper  care 
ofpoultr}'.  In  addition  to  the  general  sanitary  methods,  the 
following  rules  should  be  observed. 

(i)  Fowls  which  have  an  exudate  on  any  of  the  mucous 
membranes  of  the  head  or  which  have  come  from  flocks  in 
which  such  a  disease  exists  or  has  recently  existed,  should  not 
be  placed  among  healthy  poultry. 


^Bulletin  del' Acad.  Royale  deMed.  de  Belgique,  VIII.  (1894),  p.  380. 


PREVENTION  333 

(2 )  If  the  disease  appears  in  one  or  more  fowls  of  a  flock 
the\^  should  be  immediately  separated  from  the  well  ones.  If 
possible,  the  source  of  the  infection  should  be  determined  and 
removed . 

(3)  The  quite  common  practice  of  allowing  fowls  from 
different  flocks  to  run  together  during  the  day  should  be  dis- 
couraged. 

(4)  Care  should  be  taken  to  avoid  the  possibility  of 
bringing  the  virus  of  the  disease  from  affected  flocks  in  the  dirt 
or  excrement  which  naturally  adheres  to  the  shoes  in  walking 
through  an  infected  chicken  yard.  The  same  care  is  necessary 
in  the  interchange  of  working  implements,  such  as  ghovels, 
hoes  and  the  like. 

It  is  evident  to  any  careful  observer  that  the  fact  is  too 
often  overlooked  that  fowls,  owing  to  their  method  of  living, 
are  more  liable  to  infection  than  other  farm  animals.  This  is 
especially  true  when  they  are  allowed  to  run  at  random,  as 
they  too  frequently  are,  picking  their  living  from  the  garbage 
pile  and  barnyards,  or  securing  even  more  unwholesome  food. 
There  is  little  doubt  that  many  so-called  outbreaks  of  con- 
tagious disease  among  fowds  are  simply  enzootics  brought 
about  by  improper  care. 

The  wide  distribution,  the  large  number  of  fowls  affected 
and  the  usual  chronic  course  of  this  disease  render  it  one  of 
the  few  poultry  affections  for  which  curative  measures  promise 
to  be  of  practical  value.  Although  prevention  is  the  safest  of 
cures,  when  the  disease  is  once  introduced  as  it  is  in  a  very 
large  number  of  flocks,  the  necessity  for  remedial  treatment  is 
apparent  and  where  economy  is  to  be  considered  should  be 
recommended.  The  practice  sometimes  followed  of  destroying 
all  of  the  affected  birds  should  be  discouraged.  Although 
experiments  have  not  been  made  to  test  the  efficiency  of 
remedies  already  recommended  or  to  investigate  the  prac- 
ticability of  others,  the  testimony  of  many  practical  poultry 
raisers  is  to  the  effect  that  the  disease  is  amenable  to  treat- 
ment. The  most  certain  of  the  known  methods  of  treatment 
is  the  local  application  of  disinfectants,  among  which  a  weak 
solution  of  carbolic  acid  appears  to  be  the  most  satisfactory. 


334  INFLUENZA 

The  fact  that  the  lesions  are  so  much  exposed  renders  the  dis- 
ease especially  favorable  for  topical  applications. 

,  DESCRIPTION   OF   PLATE    VIII. 

1.  Early  stage  of  meinbraite  forniatioJi  in  the  throat  of  a  pigeon. 

2.  A  section  from  an  advanced  stage  in  which  the  uiiicosa  is  covered 
with  a  thick  grayish  necrotic  exudate. 

3.  A  later  stage  7vhere  the  exudate  has  sloughed. 

REFERENCES. 

1.  Moore.     A  preliminary  investigation    of   diphtheria    in    fowls. 
Bulletin  No.  S.     U.  S.  Bureau  of  Animal  Industry.     1S95. 

2.  Salmon.     The  diseases  of  poultry.     1899.     p.  216. 


INFLUENZA. 


Synonyms.  Epizootic  catarrhal  fever  ;  epizootic  catarrh; 
horse  distemper  ;  pink  eye  ;  mountain  fever  ;    shipping  fever. 

^  251.  Characterization.  Influenza  is  an  acute  infec- 
tious disease  characterized  by  a  rise  of  temperature  and  a  ca- 
tarrhal condition  of  one  or  more  of  the  mucous  membranes, 
more  especially  of  the  head.  One  or  more  of  the  internal 
organs  may  become  affected.  It  usually  appears  in  epizootic 
form.  It  is  a  disease  of  horses  although  asses  and  mules  are 
susceptible  and  a  few  cases  are  reported  of  its  being  transmit- 
ted to  man  and  to  dogs. 

Influenza  is  a  generic  term  employed  to  designate  a  large 
variety  of  symptoms.  A  somewhat  careful  analysis  of  its  mani- 
festations suggests  that  possibly  it  includes  a  number  of  etiolog- 
ically  distinct  diseases  /.  e.  morbid  conditions  brought  about  by 
different  causative  factors.  The  term  has  long  been  employed 
to  designate  a  considerable  variety  of  equine  epizootics  the  in- 
dependence of  which  could  not  be  established.  The  disease, 
as  it  is  seen  in  the  horse,  suggests  further  that  possibly  it  is  in 
its  beginning,  a  general  affection  because  of  the  early  rise  of 
temperature  and  that  later  in  its  course  it  becomes,  to  a 
limited  extent,  localized.  At  present,  influenza  is  restricted 
to  groups  of  symptoms  and  lesions  in  the  horse  that  are  not 


HISTORY  335 

very  unlike  those  oi  la-grippc  in  man.  Its  symptoms,  lesions 
and  sequelae  warrant  such  a  view  at  least  for  a  working 
hypothesis.  As  it  is  not  usually  fatal,  little  progress  seems  ta 
be  made  in  acquiring  knowledge  concerning  the  nature  of  its 
morbid  anatomy.  There  is  much  need  for  careful  investiga- 
tion of  this  very  common  malady. 

§  252.  History.  According  to  the  writings  of  Falke, 
influenza  was  recognized  in  ver}-  early  times.  There  is  evi- 
dence that  it  was  known  in  the  fourth  and  fifth  centuries.  It 
was  described  by  Low  in  1729  as  an  equine  epizootic  which 
had  spread  over  Southern  Europe.  It  is  also  stated  that  cases 
of  its  having  been  transmitted  to  man  had  occurred.  Gibson 
observed  it  in  1872  in  London  and  in  different  districts  of 
England.  It  raged  in  epizootics  in  1760,  1776  and  1803.  The 
disease  was  widely  disseminated  during  the  last  century.  The 
more  important  epizootics  are  reported  in  the  years  from  18 13 
to  1815,  1825  to  1827,  1836  to  1840,  1846,  1851,  1853,  1862, 
1870,  1873,  1 88 1  to  1883,  and  1890.  Anker  who  described 
influenza  in  Switzerland  in  1826  laid  stress  on  its  contagious 
nature  and  stated  that  in  his  opinion  "a  volatile  infectious 
matter  was  the  cause." 

Influenza  spread  as  an  epizootic  in  1872  to  1873  over  the 
greater  part  of  the  United  States  where  it  received  the  name  of 
"pink  eye"  (French,  Fievre  typhoidej.  It  started  in  Canada 
and  extended  south  and  west  reaching  into  British  Columbia 
to  the  north  and  Mexico  at  the  south.  The  last  great  epizootic 
raged  in  Europe  from  t88i  to  1883  during  which  time  it  is  said 
to  have  spread  over  nearly  the  whole  continent.  In  the  Prus- 
sian army,  8,434  horses  became  infected  in  1890;  2,497  io^ 
1891  ;  and  3,645  in  1892.  In  Copenhagen,  3,000  horses  suffered 
from  it  in  1890  and  1891. 

§  253.  Geographical  distribution.  Influenza  seems  to 
be  known  in  nearly  if  not  all  of  the  countries  of  Europe  and 
America.  In  certain  sections  of  the  United  States  it  is  almost 
a  constant  affection.  This  is  especially  true  of  certain  cities 
owing  to  the  constant  introduction  of  "green"  horses. 

§  254.  Etiology.  Influenza  seems  to  be  produced  by  a 
specific  infection  the  nature  of  which  has  not  yet  been  deter- 


336  INFLUENZA 

mined.  It  spreads  rapidly  among  horses.  The  virus  appears 
to  lose  its  virulence  quickly  outside  of  the  animal  body,  but 
within  the  body  it  sems  to  be  preserved  for  a  long  time. 
According  to  the  observation  of  Jensen  and  Clark,  stallions 
vi'hich  have  had  the  disease  may  transmit  it,  to  the  mares  they 
serve,  for  months  after  apparent  recovery.  Dieckerhoff  suc- 
ceeded in  transmitting  the  disease  to  healthy  animals  by  subcu- 
taneous and  intra-venous  injections  of  the  blood  of  infected 
horses,  but  Friedberger  and  Arloing  failed  to  do  so.  Horses 
are  most  susceptible.  Sex,  breed,  stable  management  and  feed- 
ing appears  to  have  little  or  no  influence  on  their  individual 
susceptibility. 

Infection  usually  takes  place  from  horse  to  horse.  The 
virus  appears  to  be  carried  by  infected  human  beings,  litter, 
harnesses  and  thermometers.  In  many  cases  one  attack  con- 
fers immunity  but  a  second  infection  or  a  relapse  frequently 
occurs.  Toward  the  end  of  an  epizootic  the  disea.se  is  usually 
milder  in  form,  probably  due  to  a  gradual  attenuation  of  the 
virus. 

§  255.  Symptoms.  The  period  of  incubation  varies 
from  four  to  seven  days  after  which  the  disease  appears  sud- 
denly, and  may  attain  its  highest  point  of  intensity  within 
twenty-four  hours.  The  organs  of  circulation,  nervous 
centers,  digestive  and  respiratory  mucous  membranes  and  con- 
junctiva are  especially  affected.  There  is  partial  or  entire  loss 
of  appetite  and  depression.  The  temperature  is  characterized 
by  a  sudden  rise  of  from  3  to  4°  F.  or  even  more.  It  remains 
high  with  but  slight  variations  for  from  three  to  six  days  and 
then  falls  rather  quickly,  often  within  twenty-four  hours,  to 
the  normal.  At  first  the  frequency  of  the  pulse  is  but  little 
increased  in  comparison  to  the  elevation  of  the  temperature, 
but  later  it  rises  to  from  60  to  70  and  in  fatal  cases  from  80  to 
100  or  more.  It  generally  continues  high  for  some  time  even 
after  the  temperature  has  fallen.  The  fever  is  characterized 
by  unevenness  in  distribution  of  the  external  temperature  of 
the  body.  The  early  rise  of  temperature,  while  the  affected 
horses  appear  to  be  healthy,  is  of  much  diagnostic  value. 


SYMPTOMS  337 

Usually  the  nervous  depression  co-exists  with  the  fever. 
The  animal  may  hold  its  head  down  and  appear  to  be  coma- 
tosed.  Extreme  muscular  debility  is  frequently  associated 
with  this  stupor.  Tremors  may  occur,  the  hind  legs  may  give 
w^a}-  while  walking  and  paralysis  of  the  hind  quarters  appears 
in  a  few  cases. 

The  oral  mucous  membrane  is  greatly  congested,  hot,  drj^ 
or  coverad  with  mucus.  There  is  sometimes  difficulty  in 
swallowing.  The  animal  frequently  yawns.  There  is  usually 
constipation  in  the  beginning  of  the  disease  w-hich  may  be 
accompanied  with  colic.  The  feces  are  formed  into  small  hard 
balls  and  are  covered  with  masses  of  mucus.  Later,  diarrhoea 
with  considerable  tenesmus  usualh'  occurs.  The  feces  are 
of  a  thin,  pulpy,  and  even  fluid  consistence,  and  sometimes 
have  a  foetid  odor.  At  the  beginning  of  the  attack  the  urine 
is  alkaline  but  it  becomes  acid  when  the  intestinal  lesions  are 
developed.  It  rarely  contains  albumin  but  desquamated  epi- 
thelial cells  of  the  bladder  are  often  present  in  large  quantity. 
A  severe  affection  of  the  eyes  is  quite  constant  and  quite  a 
characteristic  symptom  of  influenza.  At  fir.st  it  consists  chiefly 
of  catarrhal  and  later  of  phlegmonous,  conjunctivitis  with 
considerable  swelling  of  the  eyelids  which  may  be  followed  bj^ 
keratitis  and  possibly  by  an  exudative  or  hemorrhagic  iritis. 
Usually  both  eyes  are  affected.  The  first  indications  are  tears, 
intolerance  of  light,  intense  hyperemia  of  the  conjunctiva  and 
contraction  of  the  pupil.  The  eyelids  swell,  are  hot,  painful 
and  kept  more  or  less  continually  closed.  A  grey,  muco- 
purulent secretion  accumulates  between  the  eyeball  and  the 
eyelids  and  the  eyeball  becomes  very  sensitive  to  pressure. 
The  cornea  at  the  beginning  of  the  keratitis  has  a  greasy 
lustre,  is  at  first  iridescent,  later  on  exhibits  milky  opacity 
over  its  surface.  It  is  considerably  injected  with  blood  at  its 
edge  ;  the  iris  becomes  swollen  and  yellowish  in  color.  Often 
•  these  inflammatory  changes  of  the  eye  disappear  in  a  strik- 
ingh'  short  time. 

During  the  further  progress  of  the  disease,  swellings 
appear  on  the  extremeties,  sheath,  epigastrium  and  lower  part 
of  the  chest.     It  mav  be  concluded  that  these  swellings  are 


33S  INFLUENZA 

due  to  oedema  caused  by  passive  congestion.      I,ess  frequently 
the  swellings  are  of  an  inflammatory  nature.     The  swelling  of 
the  extremeties  causes   the    gait    to    be    stiff    and    unwieldy. 
Inflammation    of    the    sheaths  of    the    tendons   is   sometimes 
observed. 

The  respiratory  mucosa  are  congested.  At  first  there  is  a 
serous  and,  later  on,  a  muco-purulent  discharge  from  the  nose, 
slight  swelling  of  the  submaxillary  glands,  moderate  accelera- 
tion of  respiration  and  a  cough.  As  a  rule  the  animal  becomes 
emaciated  during  the  course  of  the  disease,  pregnant  mares 
may  abort. 

The  average  duration  of  the  disease  is  from  six  to  ten 
days,  although  severe  cases  may  run  for  two  or  three  weeks 
and  ver}'  mild  cases  may  recover  in  from  three  to  six  days. 

In  certain  cases  complications  may  arise  such  as  cardiac 
debility,  grave  cerebral  symptoms,  severe  gastro-intestinal 
inflammation,  laminitis  and  petechial  fever  all  of  which  have 
been  described  as  accompanying  complications. 

The  mortality  varies  at  different  times  and  in  different 
places.  The  average  appears  to  be  from  0.5  to  4  per  cent. 
Dieckerhoff  saw  a  loss  of  4  per  cent  among  1,700  horses; 
Aureggio,  one  of  3  per  cent  among  Soo  horses  ;  Friedberger, 
one  of  9  per  cent  ;  and  Siedamgrotzky,  one  of  10  per  cent.  It 
is  stated  that  in  1872,  in  Philadelphia,  7  per  cent  of  30,000 
infected  horses  died. 

§256.  Morbid  anatomy.  The  principal  tissue  changes 
of  influenza  are  met  with  in  the  organs  of  digestion.  The 
mucous  membrane  of  the  pyloric  portion  of  the  stomach  and 
of  the  intestines  is  hyperaemic,  swollen  and  sprinkled  with 
slight  hemorrhages.  The  submucosa  is  yellowish  in  color  and 
infiltrated  with  a  gelatinous  substance  causing  the  membrane 
to  form  thick  somewhat  translucent  elevations  containing  a 
fluid  which  coagulates.  Peyer's  patches  are  enlarged  especially 
those  in  the  neighborhood  of  the  ileo-caecal  valve.  The 
mucous  membrane  of  the  mouth  and  sometimes  that  of  the 
pharynx  show  similar  changes. 

The  mucous  membrane  of  the  upper  air  passages  is 
hyperaemic  and  swollen.      In   rare  cases,   the   mucosa   of  the 


DIFFERENTIAL    DIAGNOSIS  339 

larynx  is  inflamed.  Also  the  subcutis  when  inflammatory 
swellings  appear  on  the  skin.  Schiitz  found  that  in  the  brain 
and  spinal  cord  the  arachnoid  spaces  are  filled  with  a  fluid 
which  is  generally  clear  although  it  may  contain  leucocytes.  He 
reports  one  case  in  which  the  lateral  ventricles  contained  a 
large  quantity  (20  c.  c.)  of  fluid.  The  other  le.sions  which 
may  be  found  depend  upon  the  extent  of  localization  of  the 
disease.  Usually  there  are  slight  swelling  of  the  spleen,  small 
hemorrhages  in  the  intestines,  under  the  serous  membranes 
and  in  the  lungs,  eyes  and  brain  ;  gelatinous  infiltration  of  the 
renal  connective  tissue  and  mesentery  ;  swelling  of  the  lymph 
glands  ;  j^ellowish  serous  exudates  in  the  larger  cavities  of  the 
body  and  imperfect  coagulation  of  the  blood.  One  or  all  of 
these  changes  may  appear  in  a  single  animal. 

^257.  Differential  diagnosis.  Influenza  must  be  difi"er- 
entiated  from  strangles  and  contagious  pneumonia.  The 
differentiation  between  pleuro-pneumonia  and  influenza  is 
difficult  only  at  the  beginning,  when  merely  general  symp- 
toms, such  as  fever,  loss  of  appetite  and  weakness  are  present. 
It  .should  be  mentioned  that  the  two  diseases  maj'  affect  the 
horse  simultaneously.  When  the  skin  is  greatly  swollen,  in- 
fluenza may  resemble  petechial  fever,  from  which  it  can,  how- 
ever, very  soon  be  distinguished  by  the  absence  of  petechiae, 
by  the  mildness  of  its  course  and  its  greater  contagiousness. 
In  case  of  strangles,  the  lesions  in  the  lymphatics  may  serve  as 
distinguishing  characters.  If  abscesses  are  in  evidence  the 
finding  of  the  streptococcus  of  strangles  would  be  quite  con- 
clusive. It  would  be  positive  providing  Streptococcus  equi 
could. readily  be  distinguished  from  the  pyogenic  streptococci. 

With  these  diseases,  a  diagnosis,  save  in  the  more  typical 
forms,  is  difficult.  Without  a  definite,  recognizable,  etiological 
factor  or  other  exact  tests,  a  positive  diagnosis  in  doubtful 
cases  can  not  be  made. 

REFERENCES. 

1.  LiGNiERES.     Influenza  or  infectious  pneumonia,  the  etiology  of 
■  equine,    /our.  of  Comp.    Path  and  Therap.     Vol.  XI.     (1898).      p.  312. 

2.  M'Fadvean.     Influenza   in    the   horse,    what   is   it?     Jour,    of 
■Camp.  Path  and  Theraputics.     Vol.  II.     (1889).     p.  105. 


340  ■      ,  DOG    DISTEMPER 

3.  Marsden.  Influenza.  The  Veterinary  Journal.  New  Series, 
Vol.  II.  (1900).  p.  315.  (  M.  describes  three  forms  (i)  catarrhal  fever, 
(2)  bilious  fever,  (3)  epizootic  cullulitis). 

4.  Nelson.  Influenza.  Bulletin  22.  State  Agric.  Exper.  Station^ 
IVashingtoii.     1896. 


DOG  DISTEMPER. 


Synonyms.  Dog  plague  ;  dog  disease  ;  bench  show 
disease  ;  typhus  fever  in  the  dog  ;  typhoid  fever  in  the  dog  ; 
febris  catarrhalis  epizootica  canum. 

§258.  Characterization,  Distemper  is  an  infectious  dis- 
ease appearing  in  sporadic  cases  or  in  epizootics.  It  is  usually 
determined  by  a  rise  of  temperature,  loss  of  appetite  and  lassi- 
tude, followed  by  a  catarrah  of  the  conjtinctiva,  respiratory 
passages  and  digestive  tract. .  Frequently  there  are  serious 
disturbances  of  the  nervous  system.  It  is  the  most  important 
canine  disease.  It  is  reported  that  cats,  wolves,  foxes,  jack- 
alls,  hy'senas  and  monkeys  suffer  from  it. 

§  250.  History.  This  disease  of  dogs  was  known  in  qtiite 
early  times.  Its  historj'  shows  that  possibly  it  was  introduced 
into  Southern  Europe  from  Peru,  South  America,  about  the 
middle  of  the  eighteenth  century.  It  was  regarded  as  being 
closely  allied  to  a  number  of  diseases  of  the  human  species 
such  as  the  plague  and  typhus.  Trasbot  believed  it  to  be 
closely  allied  to,  if  not  identical  with,  small  pox. 

§  260.  Geographical  distribution.  Distemper  in  dogs 
is  a  wide  spread  disease.  It  is  exceedingly  common  in  the 
United  States  and  its  ravages  extend  throughout  America  and 
seem  to  be  no  less  in  Europe.  It  is  stated  that  there  is  no 
country  or  climate  in  which  the  dog  is  exempt  from  distemper. 

§  261.  Etiology.  The  specific  cause  of  distemper  has 
not  been  demonstrated.  A  large  number  and  variety  of 
bacteria  have  been  thought  by  different  investigators  to  stand 
in  a  casual  relation  to  this  disease.  Schantyr  stated,  in  1892, 
that  canine  distemper  should  be  divided  into  three  different 
diseases  and  that  each  is  produced  by  a  distinct  species  of 
bacteria.  More  recently  (1899)  Jess  has  isolated  a  bacillus 
from    the   catarrhal   secretions,    blood,    serous   exudates   and 


SYMPTOMS  341 

organs.  He  reports  having  reproduced  the  disease  in  dogs 
with  pure  cultures  of  this  organism.  The  writer  has  not  been 
able  to  find  this  bacillus  in  a  few  cases  which  he  has  examined, 
but  a  streptococcus  has  often  appeared  in  pure  cultures  from 
the  various  organs.  There  is  much  need  for  further  investi- 
gation into  the  etiology  of  this  malady.  That  it  is  produced 
by  a  specific  cause  is  very  clearly  indicated  by  the  reported 
results  of  investigations  to  the  effect  that  dogs  inoculated  with 
the  nasal  discharge  of  affected  animals  develop  the  disease. 

§  262.  Symptoms.  The  symptoms  appear  after  a  period 
of  incubation  of  from  four  to  six,  possibly  eight  days.  They 
vary  to  such  a  degree  that  it  is  impossible  to  refer  to  all  of  the 
manifestations.  In  some  cases  the  symptoms  suggest  a  general 
disorder.  In  others  they  are  referable  to  certain  parts  or 
organs  such  as  the  mucosa  of  the  digestive  and  respiratory 
tracts,  the  brain  or  integument.  As  a  rule  several  organs  are 
implicated. 

The  initial  symptoms  such  as  depression,  roughened  con- 
dition of  the  coat,  loss  of  appetite  and  elevation  of  temperature 
are  usually  suggestive  of  a  general  disturbance. 

In  a  large  majority  of  cases,  conjunctivitis  is  the  primary 
ocular  symptom.  Tears  flow  from  the  eyes  and  photophobia 
is  present.  The  mucous  membrane  of  the  eyelids  becomes 
highly  congested  and  swollen  and  the  eyelids  turgid.  The 
discharge  from  the  eyes  which  is  at  first  serous  soon  becomes 
mucous  and  purulent.  The  exuded  matter  consists  of  pasty 
mucous  or  dirty  yellowish  pus.  This  exudate  collects  under 
the  lower  eyelids,  chiefly  at  the  inner  canthus  of  the  eye  and 
soils  the  edges  of  the  eye  lids,  upon  which  it  frequently  dries 
into  crusts  and  causes  the  lids  to  adhere,  especially  during  the 
night.  Ulcers  form  on  the  cornea  in  consequence  of  the  action 
of  the  accumulated  and  decomposing  pus  and  the  patient  wiping 
and  rtibbing  the  eyes  with  its  paws.  The  epithelium  of  the 
cornea  sometimes  suffers  more  or  less  from  shallow  flat  lesions 
which  give  the  surface  of  a  cornea  a  rough  and  uneven  appear- 
ance. Frequently  smaller  and  deeper  ulcers  form  especially 
toward  the  center  of  the  cornea. 

In  other  cases,  there  is  a  diffuse,  parenchymatous  keratitis 


342  DOG    DISTEMPER 

which  renders  the  cornea,  to  a  considerable  extent,  opaque  and 
gives  it  the  appearance  of  ground  glass.  These  extensive 
opacities  sometimes  develop  in  a  comparatively  short  time. 
This  affection  of  the  cornea,  the  so  called  "distemper  of  the 
eyes"  is  frequently  the  onlj-  evidence  of  distemper  with  the 
exception  of  the  high  temperature. 

There  may  be  vomiting,  well  marked  congestion  and  dry- 
ness of  the  oral  mucosa.  There  is  usually  constipation  at  first, 
but  later  a  diarrhoea  in  which  the  feces,  as  a  rule,  are  very 
foetid,  often  slimy  and  froth3\  Hemorrhagic  intestinal  catarrah 
sometimes  exists.  The  urine  frequently  contains  albumin, 
especially  when  the  patient  is  weak  or  in  an  advanced  stage  of 
the  disease,  biliary  pigments  but  rarely  hemoglobin. 

The  nasal  discharge  is  serous  at  first,  mucous  or  purulent 
later  on.  It  is  followed  by  sneezing,  panting  and  nasal  pruri- 
tis,  which  causes  the  animal  to  rub  its  nose  with  its  paws. 
The  pus  discharge  from  both  nostrils  may  be  very  copious.  It 
is  sometimes  mixed  with  streaks  of  blood,  and  varies  in  color 
from  a  dirty  yellow  to  a  dirty  green.  Later,  it  may  become  foetid 
and  even  watery.     Ulcers  may  appear  on  the  nasal  mucosa. 

Laryngeal  catarrh  usually  accompanies  the  nasal  catarrh 
and  manifests  itself  by  a  cough,  which  comes  on  in  paroxysms 
and  which  is  at  first  hoarse  and  dry,  but  later  moist  and 
accompanied  by  a  discharge  of  phlegm.  The  cough  excites 
vomiting.  The  catarrh  spreads  from  the  larynx  to  the  trachea 
and  bronchi.  The  resulting  bronchitis  is  followed  by  an  in- 
creased rate  of  breathing  and  manifests  itself  by  a  cough  and 
hoarse,  sharp,  vesicular,  respirator}^  murmurs.  Frequently 
there  is  a  catarrh  of  the  mucous  membrane  of  the  smaller 
bronchi.  There  may  be  difficulty  in  breathing  and  a  feeble 
cough  which  the  patients  try  to  suppress.  The  cough  may  be 
excited  by  percussion  of  the  thoracic  walls,  by  the  animals 
getting  up  and  by  their  being  taken  out  of  their  kennels. 
Young  and  weak  animals  that  cannot  remove  the  accumulated 
phlegm  from  the  bronchi  by  coughing  become  affected  with 
catarrhal  pneumonia.  The  pneumonia  can  be  recognized  b}' 
the  increase  in  temperature. 

Distemper  often  begins,  especially  in  anaemic  animals,  with 


SYMPTOMS  343 

great  depression  and  dullness.  Strong  animals,  however,  more 
usually  exhibit  symptoms  of  acute  hyperemia  of  the  brain, 
such  as  excitement,  restlessness,  yelping  and  even  attacks  of 
furv,  which  give  way  later  on  to  manifestations  of  cerebral 
pressure.  Spasms  frequently  occur  either  generally  or  confined 
to  particular  limbs  which  swing  backward  and  forward  as  if 
affected  by  chorea.  The  animal  may  fall  down  as  if  suffering 
from  epilepsy,  bark,  become  unconscious  and  exhibit  spasms 
•of  the  muscles  generally.  The  sphincters  of  the  anus  and 
bladder  become  relaxed  and  consequently  feces  and  urine  are 
involuntarily  passed.  There  is  a  gradual  return  of  conscious- 
ness which,  in  a  short  time,  is  complete  and  the  dog  manages 
to  get  up  although  he  is  very  weak.  Such  an  epileptiform 
attack  may  pass  directly  into  long  continued  coma. 

Paralysis  may  follow  the  convulsions  or  it  may  come  on 
simultaneously  with  them.  It  seldom  occurs  at  the  beginning 
of  the  disease.  It  may  be  confined  to  certain  groups  of  mus- 
cles as  those  of  a  limb,  the  whole  of  the  hind  quarters  or  even 
the  entire  body  in  the  form  of  paresis,  especially  of  the  motor 
nerves,  combined  with  excessive  muscular  weakness.  The 
sick  dog  staggers  and  his  hind  quarters  sway  from  side  to  side 
or  he  becomes  incapable  of  supporting  himself  on  his  hind 
legs.  Frequently  he  knuckles  on  all  four  legs  and  in  severe 
cases  is  unable  to  stand.  Permanent  paresis  of  the  hind  quar- 
ters with  paralysis  of  the  bladder  and  rectum  is  a  frequent  re- 
sult of  distemper.  In  some  cases  there  may  be  paralysis  of 
the  muscles  of  the  tongue. 

A  characteristic  pustular  exanthema  is  frequently  observed 
on  the  inner  surface  of  the  thighs  and  abdomen  and  in  abortive 
cases  it  may  be  the  only  symptom  of  distemper.  It  first  ap- 
pears in  the  form  of  minute  red  spots,  which  after  twenty-four 
hours  develop  into  miliary  nodules  that  are  surrounded  by  a 
red  ring.  These  nodules  change  into  vesicles  and  pustules 
which  may  become  as  large  as  a  pea  or  bean.  They  dry  into 
a  yellowish  brown  crust  or  burst  leaving  a  raw  surface.  Heal- 
ing takes  place  with  desquamation  of  the  epidermis  after 
about  eight  days  leaving  pigmented,  pale  reddish  areas  which 
persi.st  for  some  time.      Generally,  there   are  only  a   few  pus- 


344  ^OG    DISTEMPER 

tules  present.  The  exanthema  may  spread,  in  the  form  of  a 
scabby  eczema,  over  the  whole  body,  to  the  membrane  of  the 
external  auditory  meatus  and  less  frequently  to  the  mucous 
membrane  of  the  mouth  and  eyes.  This  eruption,  contrary  to 
that  of  sarcoptic  mange,  is  accompanied  by  only  slight  pruritis. 
Intense  catarrh  of  the  prepuce  may  appear  simultaneously 
with  the  skin  eruption. 

The  temperature  which  is  usually  very  irregular,  is  higher 
during  the  initial  stage  than  when  local  manifestations  appear. 
It  often  falls  with  remarkable  rapidity  below  normal  towards 
the  approach  of  death.  If  the  disease  runs  a  protracted  course, 
the  patient  becomes  emaciated,  the  hair  loses  its  lustre,  the 
body  exhalations  have  a  very  foetid  odor,  the  eyes  are  sunken, 
the  mucous  membranes  become  pale  and  the  patient  grows 
weaker,  staggers  when  walking  or  lies  in  a  state  of  coma. 

In  abortive  cases  recovery  may  take  place  in  eight  or  ten 
days,  although  the  disease  usually  lasts  three  or  four  weeks. 
With  severe  complications,  especially  those  of  the  nervous  sys- 
tem, distemper  assumes  a  protracted  course  and  is  frequently 
followed  by  sequelae,  such  as  paralysis  and  convulsions,  which 
may  persist  for  months  and  even  longer.  The  average  mor- 
tality appears  to  be  from  50  to  60  per  cent. 

§  263.  Morbid  anatomy.  The  anatomical  changes  in 
the  respiratory  system  are  those  of  rhinitis,  laryngitis,  bron- 
chitis and  catarrhal  pneumonia.  The  nasal  mucous  membrane 
is  either  very  pale  or  greatly  congested,  swollen  and  covered 
with  a  thick,  purulent,  greyish  green  or  dull  reddish  inflam- 
matory exudate  which  is  mixed  with  coagulated  blood  and 
collects  chiefly  between  the  lamellae  of  the  turbinate  bones 
and  in  the  frontal  sinuses.  Hemorrhagic  ulcers  are  some- 
times present.  The  mucous  membrane  of  the  larynx  and 
bronchi  is  hyperaemic,  swollen,  often  infiltrated  with  hemor- 
rhages and  covered  with  pus.  vSometimes  cattarrhal  ulcers 
appear.  The  large  bronchial  tubes  often  fail  to  exhibit 
changes  which  might  have  been  expected  from  the  symptoms. 
The  smaller  bronchi  are,  on  the  other  hand,  frequentlj-  filled 
with  dirty  grey  and  even  bloody,  viscid  pus.  There  are  areas 
of  congestion  on  the  surface  of  the  lungs,  some  parts  of  which 


MORBID    ANATOMY  345 

may  contain  but  little  air.  There  may  be  areas  of  collapse  or 
those  abnormally  filled  with  air.  The  inflammatory  foci  of 
the  lungs  are  usually  consolidated.  In  very  young  animals 
there  may  be  a  fibrous  exudate  which  is  very  soft  and  which 
readily  liquifies.  The  hepatization  frequently  involves  an 
entire  lobe.  The  hepatized  parts  are  frequently  studded  with 
small  suppurating  foci,  or  are  diffusely  infiltrated  with  pus. 
The  plura  over  the  affected  parts  is  often  inflamed.  The 
bronchial  glands  are  swollen  or  infiltrated  with  a  serous  fiuid 
or  with  pus. 

In  the  digestive  system,  the  mucous  membrane  of  the 
stomach  and  intestines,  especially  that  of  the  small  intestine, 
is  hyperemic  and  swollen.  It  may  be  covered  with  a  tough 
mucus  and  often  sprinkled  with  hemorrhages.  In  other  cases 
it  is  very  pale,  swollen  and  easily  torn.  Frequently  the  con- 
tents of  the  intestine  are  blood  stained  and  the  mesenteric 
glands  enlarged  and  oedematous. 

The  brain  is  anaemic  and  often  there  is  a  serous  effusion 
into  the  lateral  ventricles  and  subarachnoid  spaces.  In  a  few 
cases  there  are  signs  of  a  purely  venous,  cerebral  hyperemia  as 
for  instance,  great  congestion  of  all  the  sinuses,  venous  plexuses 
and  vessels  of  the  pia  and  the  appearance  on  the  cut  surfaces 
of  the  brain  of  numerous  blood  points  which  can  easily  be 
wiped  off.  Kolesnikoff  found  microscopically  the  brain  sub- 
stance, especially  the  walls  of  the  vessels,  infiltrated  with 
leucocytes.  Krajewski  noticed  dilation  of  the  vessels,  cellular 
infiltration  of  their  walls,  filling  of  the  perivascular  spaces  with 
lymphoid  cells  and  migration  of  lymphoid  cells  into  the  stroma 
of  the  brain  and  into  the  protoplasm  of  the  ganglionic  cells. 
The  changes  in  the  spinal  cord,  which  are  not  well  marked, 
consist  chiefly  of  anaemia  and  slight  oedema  especially  in  the 
lumbar  region.  Mazulewitsch  states  that  in  acute  paralysis 
there  are  changes  in  the  walls  of  vessels  with  an  exudate  along 
the  vessels  and  in  the  interstitial  tissue  of  the  gray  matter  of 
the  spinal  cord.  In  chronic  distemper,  there  is  a  localized 
interstitial  myelitis  with  partial  atrophy  of  the  cord.  Hadden 
found  groups  of  emigrated  blood  corpuscles  in  it.  In  severe 
cases,  according  to  Trasbot,  the  spinal  cord  and  its  membranes 


346  DOG    DISTEMPER 

are  often  considerably  injected  with  a  sero-fibrinous  exudate  in 
and  under  the  arachnoid  and  even  into  the  substance  of  the 
spinal  cord. 

Among  the  other  changes  which  have  been  described  we 
may  mention  decrease  in  the  total  quantity  of  the  blood  of  the 
body,  combined  with  a  certain  degree  of  hydraemia.  There 
may  be  fatt}^  degeneration  of  the  liver  and  kidneys.  The  mus- 
cular tissue  of  the  heart  is  discolored  in  consequence  of  cloudy 
swelling  and  fatty  degeneration  of  its  fibers.  The  lymph 
glands  may  be  oedematous. 

§  264.  Differential  diagnosis.  Distemper  is  to  be 
differentiated  from,  (i)  A  simple  primary  catarrah,  such  as 
that  of  the  eyes,  nose,  lungs,  stomach  or  intestines.  While  the 
•differentiation  is  often  difficult  at  first,  as  distemper  frequently 
manifests  itself  in  the  following  affections,  a  single  mucous 
membrane  or  in  one  organ.  In  general  the  diagnosis  is  obtained 
from  the  epizootic  nature  of  the  disease,  age  of  the  patient, 
high  temperature,  simultaneous  implication  of  several  organs 
and  the  unfavorable  course  of  the  malady.  The  finding  of  the 
pustules  of  distemper  is  of  much  diagnostic  value.  (2)  Rabies. 
The  symptoms  of  cerebral  irritation  which  occur  at  the  begin- 
ning of  the  disease  may  give  rise  to  the  suspicion  of  rabies. 
The  characteristic  aggressive  behavior  of  animals  suffering 
from  rabies  is,  however,  absent  in  cases  of  distemper.  The 
further  course  of  the  disease  soon  enables  a  diagnosis  to  be 
made.  (3)  The  eruption  of  distemper  if  widely  distributed 
over  the  body  may  resemble  that  of  mange.  The  mild  char- 
acter of  the  pruritus,  the  presence  of  pustules  on  the  hypo- 
gastrium  and  inner  surface  of  the  thighs,  the  rapid  spreading 
of  the  exanthema  over  the  whole  body  and  the  development  of 
other  symptoms  of  distemper,  render  the  differentiation  easy. 
The  exanthema  of  distemper  and  that  of  mange,  however, 
often  occur  simultaneously  in  the  same  animal  in  which  cases 
certain  precautions  are  necessary  in  making  the  correct  diag- 
nosis. (4)  Epilep.sy.  The  epileptiform  attacks  in  distemper 
are  distinguished  from  true  epilepsy  essentially  by  their  being 
less  acute.  (5)  It  must  also  be  differentiated  from  simple 
coryza,  bronchitis,  chorea  and  paralysis. 

Until  the  specific  cause  is  found  and  can  be  availed  of  in 


CEREBRO-SPINAL    MENINGITIS  347 

making  the  diagnosis,  much  doubt  will  necessarily  exist 
respecting  the  nature  of  the  disease  where  many  of  the  symptoms 
and  lesions  are  atypical. 

§  265.  Prevention.  The  lack  of  knowledge  concerning 
the  specific  cause  has  rendered  it  impossible  thus  far  to  close 
all  channels  of  infection  but  its  spreading  can  be  checked  to  a 
considerable  degree  by  isolation  and  the  use  of  disinfectants. 
It  has  been  stated  that  the  inoculation  with  the  virus  from  very 
mild  cases,  which  produces  a  mild  attack,  will  immunize  an 
animal  for  several  years. 

REFERENCES. 

1.  Hektwig.     Krankheiteu  der  Hunde.     1881.     p.  48. 

2.  Jess.     Der  Bacillus  der  Hundestaupe.     (  Febris  catarrhalis  epizo- 
otica  Canines.  )     Cent./.  Bak.   u.  Parasitenk.  Bd.  2^.    (1899)8.541. 

3.  L/AOSSOM.     Ueber    Geschichte    and    Kontagiositat    der    Staupe. 
Dorpat.      1892. 

4.  NiCKOLDS.     Dog  distemper.     Am.   I'el.  Review.     1900.     p.  180. 


INFECTIOUS  CEREBRO-SPINAIv  MENINGITIS  IN  HORSES. 

§  266.  Characterization.  This  is  a  disease,  that  seems 
to  be  infectious  in  its  nature,  exhibiting  symptoms  referable  to 
a  disturbance  in  the  central  nervous  system.  It  is  called 
epizootic  cerebro-spinal  meningitis  apparently  because  it  often 
attacks  a  number  of  animals  in  the  same  locality.  Although 
the  literature  contains  numerous  accounts  of  its  seemingly 
contagious  nature,  an  analysis  of  the  facts  fails  to  bring  forth 
conclusive  evidence  that  it  is  ever  transmitted  directly  from 
one  horse  to  another.  In  nearly  if  not  all  outbreaks,  the  ani- 
mals affected  have  been  subjected  to  like  conditions  of  life. 
This  disease  is,  at  the  present  time,  peculiar  in  that  its  cause 
is  not  known,  that  obvious  tissue  changes  are  usually  absent, 
and  that  it  has  a  very  high  mortality. 

§  267.  Etiology.  The  cause  has  been  attributed  to  a 
great  variety  of  conditions  such  as  fermented  food,  forage 
laden  with  fungi  or  toxic  moulds,  various  unsanitary  con- 
ditions and  possibly  other  ill-defined  agencies.      It  seems  to  be 


34^  CEREBRO-SPINAL    MENINGITIS 

true  that  in  most  outbreaks  all  of  the  animals  that  suffer  have 
had  at  least  some  one  thing  in  common  either  in  surroundings, 
food  or  management.  The  bacteriological  and  other  examina- 
tions which  have  been  made  to  determine  the  cause  have  not 
resulted  in  finding  a  specific  agent.  Micrococci  and  various 
bacilli  have  been  found  associated  with  this  disease.  The 
writer  has  had  an  opportunity  of  making  a  careful  examina- 
tion of  animals  in  two  outbreaks.  In  one  of  them  all  inocu- 
lated media  and  histological  examinations  gave  negative 
results,  in  the  other  pure  cultures  of  a  colon  bacillus  were 
obtained  from  the  brain. 

§  268.  Symptoms.  The  mildest  attacks  are  manifested 
by  paresis  or  loss  of  perfect  control  over  the  limbs,  loss  of 
power  over  the  tail,  impairment  of  appetite  and  some  difficulty 
in  swallowing,  together  with  areas  of  hyperemia  and  reddish- 
brown  discoloration  of  the  orbital  and  nasal  mucosae.  In 
other  cases  paralysis  of  one  or  more  limbs  may  supervene  but 
without  marked  fever  or  coma. 

The  more  severe  forms  are  ushered  in  by  violent  tremb- 
ling, or  by  stupor,  apathy  and  extreme  muscular  weakness  or 
actual  paralysis.  In  such  cases  the  animal  may  stagger  or 
fall.  The  inability  to  swallow  is  often  a  marked  symptom,  the 
saliva  falling  in  strings  from  the  lips.  Another  common 
phenomenon  is  the  rigid  contraction  of  the  muscles  of  the 
neck,  back  and  loins,  the  parts  becoming  tender  to  the  touch 
and  a  more  or  less  prominent  opisthotonos  setting  in.  Twitch- 
ing of  the  muscles  of  the  shoulders  and  flanks  may  be  noticed. 
Trismus  is  sometimes  seen.  The  breathing  is  usually  rapid 
and  catching  and  the  temperature  ranges  from  104°  to  106°  F. 
The  pulse  may  be  accelerated  and  hard,  soft  and  weak,  or 
alternating.  The  eyes  are  usually  violently  congested,  of  a 
brownish  or  yellowish-red  color  and  the  eyeballs  may  be  turned 
to  one  side.  Paroxysms  of  delirium  may  set  in  when  the 
animal  will  push  against  the  wail  or  perform  any  of  the  dis- 
orderly movements  following  meningo-encephalitis.  Sooner 
or  later  coma  and  paralj-sis  supervene  and  death  occurs  in  from 
five  to  forty-eight  hours.  In  the  most  acute  cases  the  animal 
falls  and  dies  in  convulsions.     On  an  average  the  disease  lasts 


MORBID    ANATOMY  349 

from   eight   to   fourteen  days.      In   the  more  favorable  cases, 
improvement  may  begin  on  the  third  or  fourth  day. 

§  269,  Morbid  anatomy.  Most  writers  report  lesions  of 
leptomeningitis,  hyperemia  of  the  brain  and  spinal  cord  with 
extensive  effusion  into  the  ventricles  and  subarachnoid  spaces. 
Petechiae  and  parenchymatous  degeneration  of  the  solid  organs 
of  the  body  are  also  mentioned.  In  the  cases  examined  b}^ 
the  writer  there  has  been  an  absence  of  lesions  in  the  nervous 
system  and  other  organs  that  could  be  detected  by  a  gross 
examination.  In  one  case  the  brain,  spinal  cord  and  organs 
were  studied  histologically  with  like  results.  While  there  is 
undoubtedly  structural  changes  somewhere  in  these  organs, 
thus  far  they  seem  to  have  escaped  detection.  It  is  highly 
probable  that  up  to  the  present  time,  cases  of  uncomplicated 
meningitis  and  possibly  cerebritis  have  been  confused  with  the 
disease  in  question.  The  entire  subject  must  await  the  results 
of  further  investigation  into  both  the  etiology  and  morbid 
anatomy. 

REFERENCES. 

1.  Faville.  So-called  spinal  meningitis.  Am.  Vet.  Review. 
Vol.  XVII.     p    9. 

2.  Martin.     Cerebro-spinal  meningitis.     Ibid.    Vol.  XXI.    p.  2S9. 

3.  Sieda:\igrotzkv  and  Sehlegel.  EpizocJtic  cerebrospinal  men- 
ingitis in  the  horse.  (Abstract).  Jour.  Coinp.  Path,  and  Therapeutics. 
Vol.  IX.     p.  233. 


CORNSTALK  DISEASE  IN  CATTLE. 

§270.  Characterization.  The  name  "cornstalk  disease" 
has  been  given  to  a  somewhat  mysterious  affection  from  which 
cattle  sometimes  suffer  while  feeding  in  cornstalk  fields  late 
in  the  fall  and  early  winter.  The  meaning  generally  accepted 
and  intended  to  be  conveyed  by  this  term  is,  that  an  animal  or 
a  number  of  animals,  usually  cattle,  have  died  suddenly  after 
feeding  in  a  cornstalk  field  from  4  to  10  days.  From  a  patho- 
logical point  of  view,  therefore,  the  term  is  meaningless,  but 
it  has  served  admirably  as  a  generic  term  to  designate  certain 
fatalities  under  a  given  condition  which  are  not  easily  explained . 


350  CORNSTALK    DISEASE 

The  disease  is  very  insidious,  frequently  causing  the 
death  of  the  animals  before  its  presence  is  suspected.  Cattle 
that  act  perfectly  well  at  night  are  dead  on  the  following  morn- 
ing. Usually  all  the  animals  in  a  herd  that  die  of  this  affection 
perish  in  a  single  night  or,  at  the  longest,  within  a  few  days 
after  the  first  death  occurs.  It  is  generally  believed  to  be 
invariably  fatal  and  its  symptomatology  has  not  been  fulh- 
determined. 

§271.  History.  This  affection  of  cattle  has  been  known 
to  exist  for  many  years.  The  time  and  place  of  its  origin, 
however,  are  not  known,  but  it  seems  to  be  peculiar  to  the 
United  States  and  to  have  first  appeared  west  of  the  Alle- 
ghany Mountains.  We  are  told  of  its  occurrence  in  the  Mis- 
sissippi Valley  forty  or  more  years  ago.  It  made  extensive 
ravages  in  1864-65  and  again  in  1868.  From  an  historical 
standpoint,  no  positive  statements  can  be  made  concerning  it 
prior  to  1868,  when  the  first  recorded  investigations  into  its 
nature  and  cause  were  made.  After  that  time  the  disease 
seems  to  have  escaped  the  attention  of  investigators  until  1889, 
when  Billings,  of  the  Agricultural  Experiment  Station  ot 
Nebraska,  published  the  results  of  his  investigations. 

In  1868,  Gamgee  was  employed  by  the  United  States 
Department  of  Agriculture  to  investigate  this  disease.  The 
"  smut  theory'  "  of  its  etiology  appears  to  have  been  the  pre- 
vailing one  at  that  time  and  consequently  Gamgee's  report 
deals  almost  exclusively  with  the  effect  of  improperly  prepared 
food,  smuts  and  the  like.  Corn  smut  was  unusuallj^  abundant 
in  1868  and  he  carried  out  experiments  to  test  its  etiological 
value  with  the  conclusion  "that  smut  is  not  a  very  active 
poi.son  in  combination  with  wholesome  food." 

In  1889,  Billings  described  the  cornstalk  disease  as  an 
"  acute  extraorganismal  septicaemia,  due  to  micro-organisms 
belonging  to  the  class  of  ovoid-belted  germs,  to  which  variety 
of  disease  also  belongs  the  swine  plague,  southern  cattle 
plague,  Wildseuche,  hog  cholera,  and  yellow  fever  in  man." 
From  the  organs  of  cattle  dead  of  the  disease  he  reported  to 
have  invariably  isolated  a  bacillus  which  he  affirms  to  be  its 
cause.      He  identified  the  bacillus  which  he  found  in  the  animal 


HISTORY 


551 


tissues  with  the  one  described  by  Burrill  as  the  cause  of  a 
disease  in  cornstalks.  In  1893,  Dr.  Theobald  Smith  identified 
the  bacillus  described  by  Professor  Burrill  as  Dacillus  cIoaca\ 

Billings  also  found  pneumonia  to  be  one  of  the  lesions 
characteristic  of  this  affection  and  in  a  subsequent  bulletin  he 
places  great  importance  upon  this  lesion,  although  he  adds 
very  few  additional  observations  to  sustain  the  claim. 

In  1890,  a  few  animals  from  a  shipload  of  American  cattle 
landed  at  La  Villette,  France,  died  of  pneumonia.  They  were 
examined  very  carefully  by  Nocard  and  other  French  veterin- 
arians. From  the  diseased  lung  Nocard  obtained  a  micro- 
organism which  corresponded  very  closely  to  the  description  of 
the  bacillus  of  the  cornstalk  disease  of  cattle  described  by 
Billings  in  America.  The  publication  of  this  fact  gave  rise 
to  a  temporary  supposition  that  this  American  cornstalk  dis- 
ease might  be  a  menace  to  the  cattle  of  Europe  and  conse- 
quently initial  steps  were  taken  to  require  American  cattle  to 
be  quarantined  against  it.  The  fact  was  subsequently  deter- 
mined that  the  bacillus  isolated  by  Nocard  belonged  to  the 
espticaemia  hemorrhagica  group  of  bacteria  which  is  usually 
found  to  be  associated  with  a  form  of  bovine  pneumonia  occa- 
sionally met  with  in  America,  but  not  known  to  be  contagious, 
and  the  matter  was  dropped. 

A  single  experiment  was  made  at  Champaign,  111. ,  in  1899, 
in  which  the  etiological  importance  of  corn  smut  was  tested 
with  negative  results.  A  bacteriological  examination  of  the 
organs  from  an  animal  that  died  in  a  cornstalk  field,  supposedly 
of  this  disease,  was  made  with  negative  results  by  Professor 
Burrill  in  1889. 

In  1892,  Moore  investigated  this  disease  and  his  report 
furnishes  the  information  here  given  concerning  the  symptoms 
and  morbid  anatomy  of  this  affection. 

§  272.  Geographical  distribution.  Geographically, 
this  affection  is  restricted  very  largely  to  those  sections  of  the 
United  States  where  the  farmers  harvest  their  corn  by  picking 
the  ears  from  the  standing  stalks,  after  which  cattle  are  turned 
into  the  cornstalk  fields.  At  present,  therefore,  it  is  limited 
in  its  distribution  to  the  middle  and  northern  portions  of  the 


352  CORNSTALK    DISEASE 

Mississippi  Valley.  It  is  believed  that  there  are  exceptions  to 
this  and  that  rarely  cattle  die  from  its  effects  in  the  eastern 
part  of  the  country. 

^  273.  Etiology.  The  definite  cause  of  this  disease  has 
not  been  determined.  It  has  been  .shown,  however,  that  the 
former  theories  respecting  salt,  water  and  the  bacillus  of  the 
Burrill  disease  of  cornstalks  are  not  substantiated.  The 
hypothesis  that  the  cau.se  rests  in  the  cornstalks  themselves 
seems  to  be  the  most  tenable.  It  is  well  known  that  cattle 
rarely  if  ever  die  from  eating  cornstalks  in  moderate  quanti- 
ties. However,  the  results  of  such  investigations  as  have  been 
made  point  as  the  cause  to  an  intoxication  from  an  excessive 
quantity  of  one  or  more  elements  existing  in  the  cornstalks 
themselves. 

§  274.  Symptoms.  The  insidious  nature  and  rapid 
course  of  the  disease  usually  results  in  the  death  of  the  animal 
before  its  presence  is  detected.  In  a  few  instances,  however, 
the  sick  animals  have  been  observed  very  carefully  by  their 
owners  from  whom  all  of  our  knowledge  of  the  symptoms  is 
obtained.  One  owner  found  a  steer  lying  dow^n  and  unable  to 
rise.  His  head  was  extended,  resting  on  the  ground  and 
moving  continually  from  side  to  side  ;  this  was  kept  up  for 
several  hours,  when  he  died.  In  the  second  case  a  steer  was 
found  to  remain  behind  the  other  animals  when  they  were 
driven  to  water  about  11  a.  isr.  At  3  p.  m.  he  was  found  in  a 
dying  condition. 

Another  man  reported  that  he  found  his  animals  apparently 
well  at  5  A.  M.  At  7  A.  M.  a  heifer  was  found  resting  squarely 
upon  her  knees,  the  head  extended  and  resting  upon  the  ground. 
She  was  frothing  at  the  mouth  and  groaning  as  if  in  great 
distress.     She  died  in  about  two  hours. 

Another  report  states  that  the  sick  animals  were  dull, 
exhibited  great  weakness  and  walked  with  a  peculiar  jerky 
movement  of  the  hind  legs.  The  animals  trembled  as  if  suffer- 
ing from  a  chill.  In  a  short  time  they  fell  dowm  and  appeared 
to  be  in  great  distress,  heads  moving  continually  backward 
and  forward.  A  fourth  owner  observed  a  sick  animal  trembling 
violently  for  about  two  hours  before  it  died. 


MORBID    ANATOMY  353 

§275.  Morbid  anatomy.  In  twelve  animals  which  died 
in  cornstalk  fields  and  were  examined,  post-mortem  changes 
were  more  or  less  advanced  in  the  greater  number.  A  few 
were  examined  soon  after  death.  The  structural  changes  in 
the  organs  were  slight.  This  explains  the  .statement  of  many 
veterinarians  that  the  organs  of  cattle  dying  of  cornstalk  disease 
are  normal  in  appearance. 

The  only  gross  pathological  changes  observed  were  those 
of  a  hemorrhagic  nature.  The  hemorrhages  were  mostl}'  con- 
fined to  the  serous  membranes  and  especialh'  those  of  the 
heart.  Ecchymoses  were  more  or  less  numerous,  however, 
beneath  the  pleura  and  under  the  capsule  of  the  liver  and  of 
the  spleen.  The  mucosa  of  the  intestinal  tract  showed  areas 
in  which  the  capillaries  were  deeply  injected.  Occasionally 
there  were  hemorrhages.  In  one  case  there  were  pronounced 
hemorrhagic  areas  in  the  heart  muscle,  aorta  and  pleura.  In 
most  cases  the  liver  was  pale  in  color  and  the  acini  presented 
deep  reddish  centers  with  pale  peripheries.  The  inner  and 
middle  zones  of  the  lobules  were  more  densely  congested  than 
the  peripheral  ones.  A  layer  several  lobules  in  thickness 
immediatel}'  beneath  the  capsule  was  usually  more  engorged 
with  blood  than  the  deeper  portions  of  the  organ.  In  the  more 
densely  injected  areas  not  only  the  blood  spaces  were  filled,  but 
the  liver  cells  were  also  separated  from  each  other  by  a  space 
of  variable  width  containing  blood  corpuscles.  In  some  cases 
there  were  slight  changes  in  the  appearance  of  the  cellular 
protoplasm. 

In  all  of  the  animals  examined,  the  hemorrhages  were  of 
recent  origin  and  the  blood  normal  in  its  microscopic  appear- 
ance. There  were  no  discolored  areas  indicative  of  old  ecchy- 
moses. The  distribution  and  general  character  of  the  hemor- 
rhages, which  are  the  most  conspicuous  microscopic  lesions 
observed,  are  very  similar  to  those  described  in  certain  cases 
of  vegetable  poisoning,  more  particularly  that  of  fern  root. 

Although  certain  symptoms  described  by  the  owners  were 
referable  to  the  nervous  system,  lesions  were  not  discovered  in 
the  brain  or  spinal  cord  excepting  in  one  case  in  which  there 
was  considerable  hemorrhage  beneath  the  pia  mater. 


354  CORNSTALK    DISEASE 

In  one  animal  certain  of  the  lymphatic  glands  exhibited 
more  or  less  blood  extravasation,  particularly  in  the  interlobular 
tissue. 

§  276.  Differential  diagnosis.  This  disease  is  to  be 
differentiated  from  sudden  deaths  due  to  various  other  causes. 
As  a  rule  thej-  are  accidental  although  deaths  directly  due  to 
engorgement,  or  to  the  consumption  of  too  much  corn,  as  might 
easily  happen  during  the  first  days  that  the  cattle  are  in  the 
stalk  field.  The  diagnosis  of  the  cornstalk  disease  must,  for 
the  present,  depend  upon  the  hemorrhagic  lesions  and  the 
period  of  feeding  upon  the  stalks.  Mayo  has  pointed  out  the 
fact  that  occasionally  cattle  die  from  eating  cornstalks  exces- 
sively rich  in  nitrate  of  potash. 

Of  the  specific  infectious  diseases  which  might  be  con- 
fused with  this  affection  acute  anthrax,  symptomatic  anthrax 
and  septicaemia  hemorrhagica  should  be  mentioned.     Each  of 
these  affections  can  be  determined  from  its  specific  nature  as 
pointed  out  under  the  description  of  each  of  these  affections. 

REFERENCES. 

1.  Billings.  The  cornstalk  disease  in  cattle.  Bulletins  A^o.  7,  S. 
g  and  10.     Neb.  Agric.  Exper.  Station.     1886-8S.     p.  165. 

2.  Billings.  The  corn  fodder  disease  in  cattle  and  other  farm 
animals,  with  especial  relation  to  contagious  pleuro-pneumonia  in 
American  beeves  in  England.  Bulletins  No.  22  and  2^.  Univ.  of  Neb. 
Agric.  Ex  per.  Station.     1892. 

3.  DE  SCHWEiNlTz.  Chemical  examination  of  cornstalks  presu- 
mably the  cause  of  cornstalk  disease  in  cattle.  Bulletin  No.  10,  U.  S. 
Bureau  of  Animal  Industry.     1896. 

4.  GamgeE.  Diseases  of  cattle  in  the  United  States.  U.  S. 
Department  of  Agriculture.     1869. 

5.  Mayo.  Cattle  poisoning  by  nitrate  of  potash.  Bulletin  No.  ^g. 
Kansas  Agric.  Ex  per.  Station.     1895. 

6.  Mayo.     Cornstalk  disease  in  cattle.     Ibid.     1896. 

7.  Moore.  An  investigation  into  the  nature,  cause  and  means  of 
preventing  the  cornstalk  disease  (Toxaemia  Maidis)  of  cattle.  Bulletin 
No.  10.     U.  S.  Bureau  of  Ani)>ial  Industry.     1S96. 

8.  NoCARD.  Une  Broncho-pneumonie  infectieuse  des  Boeufs 
Americains.  The  cornstalk  disease.  Recueil  de  Medecine  Veterinaire. 
Tome  VIII.     (1891).     p.  424. 


CHAPTER    VIII. 


A  FEW  DISEASES  CAUSED  BY  ANIMAL  PARASITES. 


THE    NODULAR    DISEASE    OF    THE    INTESTINES    OF   SHEEP. 

§277.  Characterization.  The  intestinal,  nodular  disease 
•of  sheep  is  characterized  by  the  presence  of  nodules  in  the 
upper  part  of  the  large  intestine,  although  they  are  sometimes 
found  in  the  walls  of  the  ileum  and  jejunum,  varj-ing  in  size 
from  that  of  a  pin  head  to  that  of  a  bean.  They  are  caused  by  a 
nematode  and  because  of  their  tubercle-like  appearance  the 
■disease  is  often  mistaken  for  tuberculosis.  It  is  often  called 
"  knotty  "  viscera  by  butchers. 

§  278.  History.  This  disease  has  been  observed  in  the 
eastern  part  of  this  country  for  a  number  of  years.  Just  when 
it  was  introduced  does  not  seem  to  be  known.  In  18S8-9  Dr. 
Cooper  Curtice,  then  in  the  Bureau  of  Animal  Industry,  inves- 
tigated this  affection  which  up  to  that  time  was  quite  gener- 
ally thought  to  be  tuberculosis.  The  nodules  had  frequently 
been  examined  for  tubercle  bacilli,  but  with  negative  results. 
By  means  of  serial  sections  and  the  microscopic  examination 
of  the  fresh,  small  nodules,  Curtice  discovered  the  embryo  of  a 
nematode.  The  adult  was  found  in  the  intestine  in  large 
numbers.  It  was  readily  referred  to  the  genus  Oesophagos- 
toma  and  Curtice  gave  to  this  species  the  name  of  Colum- 
bianum  because  the  worm  was  first  found  in  the  District  of 
Columbia. 

§  279.  Geographical  distribution.  When  first  investi- 
_gated,  this  disease  seemed  to  be  east  of  the  Mississippi  river. 
It  was  known  to  exist  south  of  the  Potomac  river,  but  it  had 
not  been  identified  in  the  north.  It  is  now  known  to  be  more 
■or  less  prevalent  in  the  middle  and  New  England  states. 


356  NODULAR    DISEASE    IN    SHEEP 

§  280.  Etiology.  Prior  to  Curtice's  discovery,  this 
disease  was  generally  considered  to  be  tuberculosis.  He 
showed,  however,  that  it  was  caused  by  the  embryo  of  Oeso- 
phagostom a   Coin m  bia n  u m . 

The  life  history  of  this  parasite  seems  to  be  completely 
known  to  us  during  its  development  from  the  immature  form 
found  in  the  intestinal  tumors  to  the  adult  stage  ;  but  there  is 
a  period  from  the  moment  when  the  eggs  escape  from  the 
intestine  with  the  excrement  to  the  time  when  they  are 
found  in  the  intestinal  tumors  that  remains  obscure.  After 
the  embryo  has  returned  into  the  alimentary  canal  it  makes 
its  way  through  the  mucous  coat  of  the  intestine  and  becomes 
encysted  there.  Curtice  was  unable  to  learn  how  it  passes 
through  the  mucous  coat,  as  even  on  the  youngest  specimen.s 
no  sign  of  armature  is  found.  The  very  young  forms  found  in 
cysts  show  little  differentiation  beyond  what  they  could  have 
attained  in  the  shell.  They  are  .soon  surrounded  b}-  a  cyst 
which  seems  to  belong  to  them  and  to  have  been  created  b}' 
them  ;  but  whether  this  cyst  is  the  remains  of  a  molt  has 
not  been  determined.  Later  in  their  history  they  become 
surrounded  by  the  products  of  the  inflammation  they  excite  in 
the  surrounding  tissues  and  eventually  break  from  the  cyst 
and  live  in  the  cheesy  mass  of  the  tumor.  In  this  stage  of 
their  growth  the  worms  exhibit  the  intestine  and  oral  cup  and 
the  indistinct  unicellular  glands.  They  then  molt  and  show 
all  these  features  in  more  distinct  outline.  Having  attained  a 
length  of  from  3  to  4  mm.,  or  less  than  one- sixth  of  an  inch, 
they  break  from  the  tumors  to  begin  their  life  in  the  intestine. 
In  the  latter  they  continue  their  growth  and  becoming  sexualh' 
perfect,  produce  eggs  which  eventually  go  through  the  same 
cycle. 

In  developing,  this  worm  molts  at  least  three  times — once 
in  passing  out  of  the  stage  in  which  it  has  no  mouth  or  intes- 
tines, once  during  the  development  of  these  parts  as  we  find 
them  in  the  embryo  and  once  while  the  worm  changes  from 
the  embryonic  form  to  the  adult  form. 

§281.  Morbid  anatomy.  The  harm  that  these  parasites 
do  the  sheep  is  directly  dependent  on   their   numbers  and  life 


MORBID    ANATOMY 


357 


~d  -  -      -  ^ 

Fig.  69.  Cross  seclton  oj  intestine  con- 
taining nodnles.  b.  mucous  membrane,  c. 
submucosa,  d.  muscular  layers,  e.  e.  section 
through  cheesy  nodules.      (  Curtice. ) 


■histor^^  Yearlings  may  show  considerable  infection,  but  it 
is  usuall}-  in  older 
sheep  that  the  most 
abundant  infection  oc- 
curs. The  disease  is 
a  seasonal  one,  in  that 
it  can  be  found  in  best 
development  in  the 
winter.  The  lambs 
begin  to  be  infected 
in  the  summer  and  fall  and  from  that  time  the  tumors  formed 
increase  in  size  until  early  in  the  spring  of  the  next  year,  when 
they  gradually  grow  smaller  but  probably  do  not  entirely  dis- 
appear. 

A  study  of  the  fresh  tumors  by  compressing  the  smaller 
ones  between  two  glasses  and  by  dissecting  larger  .specimens 
gives  the  following  results.  The  small  tumors,  which  are 
scarcely  the  size  of  a  pinhead,  are  found  in  the  submucous 
tissue.  They  appear  like  a  .sac  filled  with  fluid  and  having  a 
little  globe  floating  within.  By  using  a  higher  magnifying 
power  the  little  globe  is  seen  to  be  a  cyst  with  a  worm  in- 
closed. By  careful  dissection  the  cyst  may  be  separated  and 
finally  the  worm  itself  may  be  removed.  In  an  older  cyst  there 
is  a  greenish,  cheesy-like  substance  present. 

When  the  little  nodules  become  larger  than  a  pinhead  and 
entirely  filled  with  the  cheesy  matter  their  structure  does  not 
materially  change,  but  is  more  difficult  to  make  out.  It  is  at 
this  stage  that  the  worm  escapes  from  the  cyst  and  begins  to 
wander  within  the  capsule  which  its  presence  in  the  tissue  has 
caused.  On  dissecting  the  large  fresh  tumors  the  worm  is 
found  in  the  ma.ss  of  cheesy  material,  which  is  now  quite 
abundant,  filling  the  cavity  and  producing  tumors  as  large  as 
the  end  of  one's  finger.  This  cheesy  material  is  usually  hard, 
dry  and  brown  at  one  end  and  soft,  yellowi.sh-green  at  the 
other.  It  is  in  this  end  that  the  worm  is  found.  If  some  of 
the  harder  nodules  are  examined,  it  may  be  found  that  there 
is  no  greenish  material   in   them   and   no  worms.     These  hard 


558  NODULAR    DISEASE    IX   SHEEP 

nodules  may  be  of  various  sizes 
and  are  found  at  all  times.  From 
these  the  worm  has  either  es- 
caped or,  in  the  case  of  the  smaller 
nodules,  the  worms  have  died. 
The  nodules  are  usually  spher- 
ical, but  the  cheesy  material  may 
appear  as  a  long  mass  or  it  may 
apparently  fill  what  seems  to  have 
^^~  been  a  worm  track.    The  last  ap- 

FiG.  70.  Section  through  ayoung  pearance  occurs  most  often  in  the 
worm  nodule.     Worm  cavity  with  small  intestines.      From  the  mu- 

worm  near  the  ce?iter.     [Curtice).  -j      x-u  j    i  ^ 

'   cous  side   these  nodules  present 

little  if  any  color.     The  older  ones  may  present  a  greenish-3'el- 

low  appearance,  especially  if  the  mucous  membrane  over  them 

is  thin.     In  well  advanced  cases,  when  the  nodules  are  numerous 

and  large,  many  are  found  in  which   the  mucous    membrane 

over  them  is  ruptured  and  the  cheesy  mass  protrudes  into  the 

intestinal  cavity.      In   these   no   worms  have  been  found  and 

hence  the  conclusion  has  been  reached  that  they  have  escaped. 

In  lambs  the  little  dots  indicating  the  presence  of  the 
young  nodules  are  very  .scattering,  but  m  older  sheep  they 
ma}'  be  very  nunierous.  Between  the  stage  in  which  a  few- 
are  scattered  here  and  there  over  the  cecum  and  that  in  which 
the  cecum  has  become  a  stiff  tube  with  walls  from  one-fourth 
to  one-half  inch  in  thickness,  there  are  all  varieties.  The 
nodules  may  extend  from  the  cecum  to  the  anus.  They  may 
also  be  abundant  along  the  small  intestine.  The  cheesy 
material  which  the  worms  produce  has  been  found  in  the 
h'mphatics,  on  the  omentum  and  in  the  liver,  but  in  these 
places  it  never  seems  to  be  sufficiently  abundant  to  show  that 
the  parasite  lived  long. 

Microscopic  serial  sections  made  from  the  alcoholic  speci- 
mens show  best  the  changes  which  have  taken  place  in  the 
surrounding  tissue.  The  worm  penetrates  to  the  submucous 
tissue  and  irritates  it.  There  is  a  special  cyst  for  the  worm 
and  a  thickened  adjoining  portion  of  the  tumor  which  is  like  a 
surrounding  membrane.     The  adjoining  cells  rapidly  increase 


DIFFERENTIAL    DIAGNOSIS  359 

in  number  so  that  the  circulation  from  the  inner  cells  is  cut 
off  and  they  die.  Their  degeneration  gives  rise  to  the  cheesy 
mass.  If  the  worm  remained  in  the  center  of  the  mass  the 
new  growth  would  eventually  cease,  but  the  worm  makes  its 
way  to  the  out.side  and  at  that  point  keeps  up  the  irritation 
and  new  growth.  This  is  shown  by  and  accounts  for  the  dried 
older  parts  of  the  larger  nodules  and  the  fresh  yellowish-green 
adjoining  parts.  As  soon  as  the  worm  escapes,  the  irritation 
ceases,  the  tumor  shrinks  and  absorption  of  the  mass  begins. 
The  irritation  produced  by  the  worm  provides  it  with  food  and 
favorable  surroundings  for  development.  Often  the  worm 
dies  from  weakness  or  other  cau.se  and  leaves  behind  those 
little  hard  incompletely-grown  nodules  which  have  been  men- 
tioned. 

The  disease  is  an  insidious  one,  for  not  only  is  the  rate  of 
infection  gradual,  increasing  slowly  in  amount  from  week  to 
week,  but  the  rate  of  development  of  the  nodules  is  very  slow, 
apparently  requiring  months.  It  is  only  w^hen  the  disease  is 
well  advanced  that  its  cumulative  effects  can  be  noticed. 

^  282.  Differential  diagnosis.  The  diagnosis  of  this 
parasitic  disease  can  only  be  made  from  a  post-mortem  exami- 
nation. In  the  living  sheep  there  may  be  .signs  of  general 
debility,  bloodless  lips  and  eyes,  thin  sides  and  flanks  and  dry 
wool.  It  may  be  that  the  flock  is  not  in  good  condition  ;  and 
in  severe  cases  the  diarrhoea  and  emaciation  may  be  excessive. 

The  only  disease  with  which  this  can  be  readily  confused 
is  tuberculosis,  which  is  very  rare  in  sheep.  A  careful  exami- 
nation of  the  lesions  will  reveal  the  presence  of  the  nematode 
which  will  decide  the  diagnosis.  The  fact  that  the  lesions  are 
usually  restricted  to  the  intestinal  wall  and  that  the  nodules 
are  sharply  circumscribed  from  the  normal  tissue  aid  in  the 
diagnosis  from  the  gross  specimen.  It  is  important  that  this 
quite  common  disease  should  not  be  diagnosed  as  tuberculosis. 

§  283.     Prevention.     For  this  disease  there  is  no  remedy 
■except  the  removal  and   extermination   of  the  adult   worms. 
They  are  usually  buried  deeply  in  the  mucous  secretions  of 
the  intestinal  mucosa  to  which  they  are  attached.     They  may 
iDe  found  in  considerable  numbers  in  old  sheep.      The  medi- 


360  NODULAR    TAENIASIS    IN    FOWLS 

cinal  remedy  must,  therefore,  be  one  which  will  remove  them. 
It  is  possible  that  such  a  remedy  may  eventually  be  found,  but 
at  present  it  is  not  known.  It  is  possible  that  some  of  the 
more  reliable  remedies  advised  for  other  intestinal  parasites 
will  do  for  these.  The  killing  of  the  adults  will  of  course 
lesson  the  number  of  eggs  with  which  the  sheep  become 
infested.  As  the  eggs  pass  to  the  ground  the  sheep  may  get 
them  either  while  grazing  or  in  their  drinking  water.  The 
same  care  in  changing  pastures,  in  providing  good  drinking 
water  and  a  plentiful  supply  of  salt,  should  be  observed  as  for 
the  prevention  of  other  parasites.  Judicious  fall  and  winter 
marketing  of  infested  sheep  will  also  tend  to  lesson  the  chances- 
of  additional  infection.  If  pasturesare  known  to  be  perma- 
nently infested,  the}'  should  not  be  used  for  sheep. 

§  284.  Nodular  intestinal  disease  of  cattle.  Cattle 
suffer  from  a  like  parasitism,  but  from  a  different  species  of 
OesopagostaDia.  In  the  bovine  species  the  nodules  are,  as  in 
sheep,  more  conspicuous  from  the  serous  surface  of  the  intes- 
tine than  from  the  mucosa.  They  are  important  in  that  fre- 
quently they  have  been  diagnosed  as  nodules  of  tuberculosis. 
As  their  structure  is  quite  like  those  in  sheep,  the  differential 
diagnosis  can  be  easily  made.  If  there  is  doubt,  serial  .sec- 
tions of  a  small  nodule  will  usually  reveal  the  presence  of  the 
worm.  In  cattle  the  oesophagostoma  nodules  do  not  appear  to 
be  of  much  if  any  importance  in  the  animal  economy. 

REFERENCES. 

Curtice.     The  nodular  disease  of  the  intestines  of  sheep.     Animal 
Parasites  of  Sheep.     U.  S.  Bureau  of  Animal  Industry.      1890.      p.   165. 


NODUIvAR  TAENIASIS  IN  FOWLS. 

S  285.  Characterization.  Nodular  taenia.sis  in  fowls  is 
a  disease  of  the  intestines  characterized  by  nodules  varying  in 
size  from  that  of  a  pinhead  to  a  small  pea  situated  either 
beneath  the  mucosa,  within  the  muscular  walls  or  in  the  sub- 
serous tissue.     It  is  caused  by  a  small  cestode. 


HISTORY  361 

^  286.  History.  In  1881,  Plana  described  a  disease  of 
the  intestines  of  fowls  in  Italy  due  to  the  presence  of  Taenia 
bothrioplitis.  His  article  deals  more  with  the  anatomy  and 
classification  of  the  cestode  than  with  the  character  of  the 
lesions  it  produced.  However,  he  illustrates  the  nodules  and 
heads  of  the  tapeworms  in  the  intestinal  wall. 

In  1894,  this  disease  was  encountered  in  some  fowls  that 
were  affected  with  diphtheria  and  that  were  under  observation 
in  the  Bureau  of  Animal  Industry.  The  following  year  the 
disease  was  briefly  described. 

§  287.  Geographical  distribution.  The  extent  of  the 
distribution  of  this  disease  does  not  seem  to  be  recorded.  It 
had  appeared  in  fowls  from  North  Carolina,  Virginia  and  the 
District  of  Columbia  at  the  time  it  was  described  and  .since 
then  a  disease  has  been  reported  from  the  Eastern  part  of  the 
State  of  New  York  and  from  Ohio  which  appears  to  be  identi- 
cal with  it.  As  the  inquiry  into  the  cause  of  poultry  diseases 
becomes  more  general,  it  is  probable  that  this  affection  will  be 
occasionally  encountered,  and  unless  its  nature  is  recognized  it 
may  lead  to  an  unwarranted  destruction  of  property. 

^  288.  Etiology.  As  first  pointed  out  by  Plana,  the 
nodules  are  produced  by  a  cell  infiltration  caused  by  the  irrita- 
tion of  the  head  of  a  small  cestode.  Piana  identified  it  as 
Tcrnia  bothrioplitis  but  Stiles  places  it  as  Davaimr  tetragona. 
There  seems  to  be  no  other  para.site  of  fowls  capable  of  pro- 
ducing such  lesions. 

§  289.  Symptoms.  The  only  evidence  of  the  disease, 
which    is    not    characteristic    of   this    affection,    is    a    general 

emaciation. 

§  290.  Morbid  anatomy.  The  lesions  described  for 
this  disease  are  restricted  to  the  intestinal  wall.  All  of  the 
fowls  described,   affected  with  this  malady,  were  from  one  to 

three  years  old. 

The  nodules  are  invariably  more  numerous  in  the  lowest 
third  of  the  small  intestine.  They  occasionally  appeared,  how- 
ever, in  small  numbers  in  both  the  duodenum  and  colon.  The 
larger  and  to  all  appearances  older  nodules  are  found  in  the 
ileum  near  the  caeca. 


362 


NODULAR    TAEXIASIS    IN    FOWLS 


#?:'S»^' 


^Ji 


:.'>;i&'5.^- 


In  the  badly 
affected  portion, 
the  nodules  give 
the  appearance  of 
closely  set  pro- 
tuberances, var}'- 
ing  in  size  from 
barely  perceptible 
areas  of  elevation 
to  bodies  4  mm. 
in    diameter.       In  Fig.  71.     Cross  sections  of  the  affeded  intestine 

some    inst  a  n  c  e  s   ^^^'^^"^S  modules,  also  attached  zvorm. 

they  appear  to  overlap  one  another.  When  separated  by  a 
band  of  normal  tissue,  they  are  round  or  somewhat  lenticular 
in  form.  In  the  latter  ca.se,  the  long  diameter  is  usually 
transver.se  to  the  long  axis  of  the  intestine.  The  larger 
nodules  are  of  a  pale  or  dark  yellowish  color,  while  the 
smaller  ones  vary  in  shade  from  the  more  highly  colored 
areas  to  the  neutral  gray  of  the  normal  serosa.  To  the  touch 
they  give  the  sensation  that  would  be  expected  if  the  sub- 
serous and  muscular  coats  were  closely  studded  with  small, 
oval,  .solid  bodies.  The  mucosa  presents  similar  elevations. 
Attached  to  the  mucosa  over  the  nodules  are  a  number  of  tape- 
worms. There  are  also  in  the  more  advanced  cases  small 
(0.5  to  I  mm.)  areas  over  the  larger  nodules  from  which  the 
mucosa  has  sloughed  leaving  small  ulcerated  depressions. 

The  larger  nodules  contain  a  greenish-yellow,  necrotic 
substance  which  appears,  in  the  advanced  stages,  as  a  seques- 
trum with  a  roughened  surface.  On  section  it  has  a  glisten- 
ing, homogeneous  appearance.  Surrounding  the  necrotic  sub- 
stance is  a  thin  layer  of  infiltrated  tissue.  The  smaller  nodules 
contain  a  more  purulent-like  substance  and  the  smallest  appear 
to  the  naked  eye  as  areas  of  infiltration.  Sections  of  the  affected 
intestine  show  upon  microscopic  examination  that  the  heads 
of  the  tapeworms  have  penetrated  the  mucous  membrane 
and  are  situated  in  different  layers  of  the  intestinal  wall. 
They  are  frequently  ob.served  between  the  villi.  As  would  be 
expected   the  heads  are  not  readily  detected   in  the  masses  of 


DIFFERENTIAL    DIAGNOSIS 


363 


necrotic  tissue  contained  in  the  larger  nodule.s,  but  they  are 
almost  invariably  found  in  the  smaller  ones.  In  a  few  sections 
the  tapeworm  has  been  traced  through  the  mucosa  to  the 
nodule  in  the  muscular  tissue  in  which  its  head  appeared.  In 
the  earlier  stage  of  the  nodular  development,  there  is  a  cell  in- 
filtration about  the  head  of  the  worm.  This  process  continues 
until  the  infiltrated  tissue  reaches  a  considerable  size. 

A  larger  form  is  commonly  found 
in  the  intestinal  contents.  Although 
macroscopically  they  appear  to  be  dif- 
erent,  Dr.  Stiles  has  found  that  they 
are   presumably  of  the  same  species. 

§  291.  Differential  diagnosis. 
Tuberculosis  is  the  only  known  dis- 
ease for  which  this  affection  is  liable  to 
be  mistaken  and  it  is  of  much  impor- 
tance that  the  two  diseases  should  not 
be  confounded.  The  diagnosis  has 
not  in  ni}'  experience  been  difficult,  as 
in  every  case  the  attached  tapeworms 
were  readily  detected  upon  a  close  ex- 
amination of  the  intestinal  contents,  pj(^_  -2.  (/)  Cross 
or  of  the  mucous  membrane  of  the  section  of  a  nodular  con- 
infected  portion  of  the  intestine. 
However,  the  worms  are  quite  small 
and  could  easily  be  overlooked  in  a 
hurried  or  cursory  examination.  In 
case  of  doubt,  if  the  affected  intestine  worm  between  villi  and 
is  opened,  and  the  mucous  surface  hooks  zvithin  the  muscle. 
washed  carefully  in  a  gentle  stream  of  water,  the  small  worms 
will  be  observed  hanging  to  the  mucous  membrane.  This 
discovery,  in  the  absence  of  lesions  in  the  liver  or  other 
organs,  would  warrant  the  diagnosis  of  the  tapeworm  disease. 
Although  much  is  written  concerning  tuberculosis  in  fowls, 
the  investigations  of  poultry  diseases  in  America  thus  far  show 
that  it  is  not  common  among  fowls  in  this  country. 


taining  necrotic  cheesy  tis- 
sue. ( 2 )  Cross  section  show- 
ing beginning  of  necrotic 
mass  about  head  of  a  tape 
worm,   (j)  Section  shoiving 


364  TRICHINOSIS 

REFERENCES. 

I.     Moore.     A  nodular  taeniasis  in   fowls.     Circular  No.  j,  U.  S. 
Burea  u  of  A  n  inial  Industry.     1 895 . 

2-     PiANA.     Mem.  della  Accademia  della  Sc.  Dell  islitntodi  Bologna 
-Ser.  4,  7,  II.     (i88o-8r).     p.  387.    • 

3.     Stiles.     Bulletin  No.   12,  U.  S.  Bureau  of  Animal  Industry. 
1896.     p.  49. 


TRICHINOSIS. 


§  292.      Characterization.       Trichinosis    is    the    disease 
<:aused   by    the   infesting  of   the    muscles   of   the    body    with 
Trichinella  spiralis.      It  affects  man,  swine  and  rats. 

§293.  History.  In  1835.  Paget,  a  medical  student,  found 
in  a  cadaver  in  a  London  dissecting  room  certain  small  worms 
which  were  described  by  Prof.  Owen  as  Trichina  spiralis.  In 
the  United  States  this  parasite  was  observed  in  a  negro  in 
Cliarleston,  S.  C,  by  Chazal  in  1841-2  and  in  the  muscles  of  a 
human  cadaver  in  Boston  by  Bowditch  in  1842-3-4.  Stiles 
finds  that  about  900  cases  have  been  reported  in  man  in  this 
country.  In  1847,  Liedy  found  the  same  species  of  worm  in 
the  muscles  of  American  swine.  Herbst  of  Gottingen  appears  to 
have  been  the  first  to  make  an  experimental  inquiry  into  the  life 
history  of  this  parasite.  In  i860,  Zenker  showed  it  to  be  the 
<^ause  of  the  disease  which  has  since  been  named  trichinosis, 
and  which  prior  to  his  observations  had  been  confounded  with 
typhoid  fever  and  other  maladies.  The  brilliant  observations 
and  experiments  of  Zenker,  Leuckart,  Virchow  and  others 
have  given  us  detailed  data  concerning  the  life  history  and 
channels  of  infection  of  this  parasite  with  the  symptoms,  dura- 
tion of  the  disease,  clinical  details  and  the  preventive  measures 
to  be  adopted.  During  the  years  i860  to  1866,  a  number  of 
outbreaks  of  trichinosis  were  experienced  in  certain  European 
States  more  particularly  Prussia  and  Saxony. 

§  294.     Description  and  life   history   of  the  parasite. 

Trichi7iella  spiralis  is  a  minute  worm,  the  male  a  little  over  i 

mm.  long,  the  female  about  3  mm.  in  length.      In  the  adult  or 

sexual  condition,  it  lives  in  the  intestine  of  man,  the  pig  and 

■other  mammals.      Internal  impregnation  takes  place,  the  eggs 


TRICHINELLA    SPIRALIS 


365 


develop  in  the  uterus  of  the  female  and  the  minute  young  to 
the  number  of  at  least  a  thous- 
and are  born  alive.     Soon  after 
birth,  the  young  worms  migrate 
through   the   walls  of  the  intes- 
tine   and,   following   the    course 
of  the  connective  tissues,   reach 
the    voluntary    muscles   of    the 
host,  such  as  those  of  the  limbs, 
back,    tongue,    muscles    of    the 
diaphragm    and    others.       Each 
worm    then    penetrates   the  sar- 
colemma  of  the  muscle  fiber  and 
coils  itself  up  in  the  muscle  sub- 
stance.   A  spindle  shaped  cyst  is 
formed  around  it,  and  the  muscle 
undergoes  more  or  less  degenera- 
tion.    This  process  gives  rise  to 
various  morbid  symptoms  in  the  p^^^    -,,      Encapsulated  Tri- 

host  but,  after  some  months  the  chinella  spiralis  in  striated  mus- 
cysts  become  calcified  and  the  ^le.  X  60.  (After  Leuckart. ) 
daneer  to  the  infested  individual  is  over.  The  flesh  of  a 
"trichinized"  human  subject  has  been  estimated  to  contain 
100,000,000  and  that  of  an  infested  pig  85,000  encysted 
worms  to  the  ounce.  In  order  that  further  development  of 
the  encysted  and  sexless  trichinae  should  take  place,  it  is 
necessary  for  the  infested  flesh  of  the  host  to  be  eaten  by 
another  animal  in  which  the  worm  is  capable  of  living,  c.  g., 
that  of  man  by  a  pig  or  rat,  or  that  of  a  pig  by  man.  When 
this  is  done  the  cysts  are  dissolved  by  the  digestive  juices,  the 
worms  escape,  develop  reproductive  organs  and  copulate,  the 
young  migrating  into  the  muscles  and  producing  the  disease 
as  before.  The  result  of  eating  an  ounce  of  "trichinized" 
pork,  improperly  cooked,  might  be  the  liberation  in  the  intes- 
tine of  perhaps  80,000  worms,  and  if  half  of  these  were  females, 
each  producing  1,000  embryos,  some  40,000,000  worms  would 
shortly  begin  to  migrate  into  the  muscles  and  produce  the 
various  symptoms  of  "trichinosis." 


o 


66  TRICHINOSIS 


It  will  be  noticed  that  in  this  case  the  parasite  is  able  to^ 
exist  in  various  hosts,  and  that  both  sexual  and  asexual  stages 
are  passed  in  the  same  host.  The  parasites  are  dispersed  by 
the  flesh  of  an  infested  animal  being  eaten  uncooked  by  au 
uninfested  one,  either  of  the  same  or  of  a  different  species. 

§  295.  Manner  of  infection.  The  danger  of  human 
infection  depends  entirely  upon  the  mode  of  preparation  of  the 
flesh.  Thorough  cooking,  so  that  all  parts  of  the  meat  reach 
or  closel}^  approach  the  boiling  point,  destroys  the  parasites. 
The  frequency  of  the  disease  in  different  countries  is  referable, 
therefore,  largel}-  to  the  habits  of  the  people  in  the  preparation 
of  pork.  In  North  Germany  where  raw  ham  and  wurst  are 
eaten  freely,  the  greatest  number  of  ca.ses  have  occurred.  In 
South  German}',  France  and  England  cases  are  rare.  In  this 
country  the  greatest  number  of  persons  attacked  have  been 
those  who  eat  raw  or  slightly  cooked  meat.  Salting  and 
smoking  of  the  flesh  as  practiced  in  this  country  are  believed 
to  be  sufficient  to  destroy  the  parasite.  There  may  be  excep- 
tional cases.  Carl  Fraenkel  states  that  it  is  very  doubtful  if 
any  cases  of  trichinosis  in  Germany  have  been  caused  by 
American  pork.  It  is  stated  that  Germany  has  yet  to  show  a 
single  case  of  trichinosis  due  to  pork  of  unquestioned  Ameri- 
can origin. 

Swine  become  largely  infested  according  to  Stiles  from 
eating  rats.  He  made  a  careful  investigation  of  this  subject 
and  found  that  the  rats  about  country  slaughter  houses  were 
infested  to  a  large  degree  with  trichinella.  Hogs  are  fed  in 
large  numbers  on  the  offal  and  they  also  frequently  devour 
the  rats. 

§  296.  Frequency.  The  dissecting  room  and  post-mor- 
tem statistics  show  that  from  one-half  to  two  per  cent  of  all 
human  bodies  contain  trichinella.  The  disease  often  occurs  in 
epidemics,  a  large  number  of  persons  being  infested  from  a 
single  source. 

In  swine  the  frequency  of  this  parasite  varies,  but  from 
one  to  three  per  cent  of  the  hogs  whose  muscles  are  examined 
microscopically  contain  trichinella. 


SYMPTOMS  367 

§297.  Symptoms.  The  ingestion  of  trichiiious  flesh  is 
not  necessarily  followed  by  disease.  When  a  limited  number 
of  the  encysted  larvae  are  eaten,  only  a  few  embryos  pass  to 
the  muscles  and  may  cause  no  symptoms.  Well  characterized 
cases  in  the  human  subject  present  two  groups  of  symptoms, 
one  referable  to  gastro-intestinal  disturbances  and  the  other  to 
the  general  infesting  of  the  muscles. 

The  following  symptoms  are  described  by  Osier.  In  the 
course  of  a  few  days  after  eating  the  infested  meat  there  are 
signs  of  gastro-intestinal  disturbance,  pain  in  the  abdomen, 
loss  of  appetite,  vomiting  and  sometimes  diarrhoea.  The  pre- 
liminary symptoms,  however,  are  by  no  means  constant,  and 
in  some  of  the  large  epidemics,  cases  have  been  observed  in 
which  they  have  been  absent.  In  other  cases  the  gastro- 
intestinal features  have  been  marked  from  the  outset,  and  the 
attack  has  resembled  cholera  nostras.  Pains  in  different  parts 
of  the  body,  general  debility  and  weakness  have  been  noted 
in  some  of  the  epidemic  cases. 

The  invasion  symptoms  develop  between  the  seventh  and 
twelfth  day,  sometimes  not  until  the  end  of  the  second  week. 
There  is  fever  except  in  very  mild  cases.  Chills  are  not  com- 
mon. The  thermometer  may  register  102  or  104°  F.  and  the 
fever  is  usually  remittent  or  intermittent.  The  migration  of 
the  parasites  in  the  muscles  excites  a  more  or  less  intense  my- 
ositis, which  is  characterized  by  pain  on  pressure  and  move- 
ment and  by  swelling  and  tension  of  the  muscles.  The  limbs 
are  placed  in  the  position  in  which  the  muscles  are  in  the  least 
tension.  The  involvment  of  the  muscles  of  mastication  and  of 
the  larynx  may  cause  difficulty  in  chewing  and  swallowing. 
In  severe  cases  the  involvment  of  the  diaphragm  and  intercos- 
tal muscles  may  lead  to  intense  dyspnea  which  sometimes 
proves  fatal.  Oedema,  a  feature  of  great  importance,  may 
appear  early  in  the  face.  Later  it  develops  in  the  extremeties 
when  the  swelling  and  stiffness  of  the  muscles  are  at  their 
height.  Profuse  sweats,  tingling  and  itching  of  the  skin,  and 
in  some  instances  urticaria,  have  been  described.  The  general 
nutrition  is  much  disturbed  and  the  patient  becomes  emaciated 
and  often  anaemic,    particularly    in    protracted    cases.       The 


•;68  TRICHINOSIS 


patellar  tendon  reflex  may  be  absent.  The  patients  are 
usually  conscious,  except  in  cases  of  very  intense  infestion  in 
which  delirium,  dry  tongue,  and  tremors  give  a  picture  similar 
to  that  of  typhoid  fever.  In  addition  to  the  dyspnea  present 
in  most  cases,  there  may  be  bronchitis,  and  in  the  fatal  cases 
pneumonia  or  pleurisy.  In  some  epidemics  polyuria  has  been 
a  common  symptom.     Albuminuria  is  frequent. 

The  intensity  and  duration  of  the  symptoms  depend  en- 
tirely upon  the  grade  of  infestion.  In  mild  cases  recovery  is 
complete  in  from  ten  to  fourteen  days.  In  severe  forms  con- 
valescence is  not  established  for  from  six  to  eight  weeks,  and 
it  may  be  months  before  the  patient  recovers  the  muscular 
strength.  One  case  in  the  Hedersleben  epidemic  was  weak 
eight  years  after  the  attack. 

Of  72  fatal  cases  in  the  Hedersleben  epidemic  the  greatest 
mortality  occurred  in  the  fourth,  fifth  and  sixth  weeks  ;  namely, 
52  cases.  Two  died  in  the  second  week  with  severe  choleraic 
symptoms.  The  mortality  has  ranged  in  different  outbreaks 
from  one  or  two  per  cent  to  thirty  per  cent. 

The  anatomical  changes  are  said  to  be  chiefly  in  the 
voluntary  muscles.  In  the  early  stages  the  muscles  look 
normal,  but  in  the  fourth  or  fifth  week  grayish-white  areas 
appear  in  which  the  muscle  fibers  are  extensively  degenerated 
Bnd  in  the  neighborhood  of  the  trichinella  there  is  an  acute 
interstitial  myositosis.  Cohnheim  has  described  a  fatty  degen- 
eration of  the  liver  and  enlargement  of  the  mesenteric  glands. 
At  the  time  of  death  in  the  fourth  or  fifth  week  or  later  the 
adult  trichinella  are  still  found  in  the  intestines. 

The  prognosis  depends  upon  the  quantity  of  infested  meat 
which  has  been  eaten  and  the  number  of  trichinella  which 
mature  in  the  intestines.  In  children  the  outlook  is  more 
favorable.  Early  diarrhoea  and  moderately  intense  gastro- 
intestinal symptoms  are,  as  a  rule,  more  favorable  than  con- 
stipation. 

§  298.  Diagnosis.  The  disease  should  always  be  sus- 
pected when  a  large  birthday  party  or  Fest  among  Germans  is 
followed  by  cases  of  apparent  typhoid  fever.  The  parasites  may 
be  found  in  the  remnants  of  the  ham  or  sausages  used  on  that 


DIAGNOSIS  369 

occasion.  The  worms  may  be  discovered  in  the  stools.  To  find 
the  worms,  a  portion  of  the  feces  should  be  spread  on  a  glass 
plate  or  black  background  and  examined  with  a  low  power  lens. 
The  trichinellae  if  present  will  appear  as  small,  glistening,  sil- 
very threads.  In  doubtful  cases  the  diagnosis  may  be  made  by 
the  removal  of  a  small  fragment  of  muscle.  A  special  harpoon 
has  been  devised  for  this  purpose  by  means  of  which  a  small 
portion  of  the  biceps  or  of  the  pectoral  muscle  may  be  readily 
removed.  Under  cocaine  anaesthesia  an  incision  may  be  made 
and  a  small  fragment  removed.  Trichinosis  may  be  mistaken 
for  acute  rheumatism,  particularly  as  the  pains  are  severe 
on  movement,  but  there  is  no  special  swelling  of  the  joints. 
There  is  tenderness  in  the  muscles  both  on  pressure  and  on 
movement.  The  intensity  of  the  gastro-intestinal  symptoms 
in  some  cases  has  led  to  the  diagnosis  of  cholera.  Many  of 
the  former  epidemics  were  doubtless  diagnosed  as  typhoid 
fever.  The  pains  in  the  muscles,  swelling,  oedema  and  short- 
ness of  breath  are  the  most  important  diagnostic  points. 

It  is  practically  impossible  to  diagnose  this  affection  in 
living  swine  except  by  removing  bits  of  infested  muscle  for 
microscopic  examination. 

§  299.  Prevention.  It  is  not  definitely  known  how 
swine  became  diseased.  It  has  been  shown  by  Stiles  that  they 
are  infested  largely  from  rats  about  slaughter-houses,  which 
are  infested  from  eating  portions  of  trichinous  flesh  of  swine. 
It  is  very  likely  that  hogs  fed  upon  offal  become  infested. 
Swine  should,  as  far  as  possible,  be  grain  fed  and  not  be 
allowed  to  eat  offal.  For  the  human  subject  the  surest  pre- 
vention is  the  thorough  cooking  of  all  pork  and  sausages. 

REFERENCES. 

Wii^LiAMS.     The   frequency   of    trichiniasis   in   the  United  States. 
Journal  of  Medical  Research.     Vol.  VI.     (1S92).     p.  64. 


APPENDIX. 


DISINFECTION. 


§  300.      Disinfection.      By  disinfection  is  meant  the  des- 
truction of  infectious  disease  producing  organisms.     For  this 
purpose,   nature    has    provided    very    important    agents   such 
as   sunlight   and   drying,  but  these   are  not   available  or  suffi- 
cient to  destroy  all  infecting  bacteria  in    all    infected    places 
within  the  necessary  time   limits.     To   supplement   these  nat- 
ural forces,  a  large  number  of  chemical  substances,  possessed 
of   germicidal    powers,  have  been    brought   into  service.      If, 
however,  the  results  of  the  test  experiments  with   these  dif- 
ferent substances  are  reviewed,  one  is  impressed  with  the  dis- 
crepancies, if  not  contradictory  conclusions,  recorded  concern- 
ing th'eir  value.      In  view  of  these  facts   the  practitioner  is 
often  at  a  loss  to  know  just  what  chemicals  to  use,   or  how  to 
apply  them  under  different  conditions  and  for  the  destruction 
of  different  species  of  organisms.     The  failure   resulting  from 
the  many  efforts  to  disinfect  stables,  pens,  kennels  and  yards 
has   caused    much    skepticism    concerning    the    efficiency    of 
many  reported  disinfectants.      In  order  to  rightly  understand 
the  reason  for  the  differences  in  results  of  the  test  experiments 
or  the  lack  of  uniformity  in  the  application  of  the  various  dis- 
infecting substances,    it  is  well  to  take  into  account  certain 
fundamental  facts. 

I.  The  bacteria  used  by  different  investigators  to  test  the 
efficiency  of  certain  substances  have  not  been  the  same.  The 
vital  resistance  of  the  various  species  is  very  different.  The 
results  obtained  in  testing  disinfectants  on  the  spirillum  of 
Asiatic  cholera  or  the  bacterium  of  bubonic  plague  give  but 
little  information  relative  to  the  value  of  the  same  disinfectants 
when  used  for  the  destruction  of  the  bacteria  of  glanders, 
tuberculosis  or  hog  cholera.     Thus  the  difficulty  in  accepting 


DISINFECTION  37 1 

the  results  of  many  of  the  older  experiments  is  that  test 
organisms  were  used  which  are  very  unlike  those  for  which 
these  disinfectants  are  now  wanted.  The  practical  value  of 
the  more  recent  experiments  is  greater  because  they  have  more 
generally  dealt  with  species  of  bacteria  with  which  most  of  the 
work  of  disinfection  has  to  do. 

2.  The  power  of  resistance  of  the  same  species  of  bac- 
terium varies  greatly  under  different  conditions.  For  instance, 
Bear  found  that  a  freshly  inoculated  culture  of  the  bacterium  of 
diphtheria  was  destroyed  with  1:5000  of  nitrate  of  silver,  but 
that  a  twenty-four  hour  culture  required  i :  1000  of  the  same 
agent  to  kill  it  in  the  same  space  of  time.  In  some  work  done 
by  Esmarch  he  made  use  of  anthrax  spores  from  seventeen 
different  sources.  They  were  destro3-ed  by  steam  at  212°  F. 
in  from  one  to  twelve  minutes  and  by  a  five  per  cent  solution 
of  carbolic  acid  in  from  two  to' forty-two  days. 

3.  The  medium  in  which  the  bacteria  exists  influences 
the  results  of  the  disinfectants.  The  bacterium  of  tuberculosis 
from  an  aqueous  suspension  dried  upon  threads  may  be 
promptly  destroyed  by  mercuric  chloride,  but  in  fresh,  puru- 
lent, tuberculous  discharges  it  cannot  be  trusted  to  destroy 
them.  Again  Behring  saj's  that  sporeless  anthrax  bacteria  in 
water  are  killed  by  corrosive  sublimate,  i  :  500,000  ;  in  bouillon, 
by  I  :  40,000  ;  but  in  blood  serum  not  with  certaint}'  with  a 
solution  of  I  :  2000.  Some  disinfectants  are  influenced  very 
much  by  the  character  of  the  material  which  contains  the 
infectious  organism,  while  other  disinfectants  are  influenced  to 
a  comparatively  slight  degree.  The  experimental  work  which 
does  not  take  the  influence  of  the  media  upon  the  disinfectant 
into  account  is  not  of  much  practical  value  and  failures  are  to 
be  expected  in  the  work  of  the  disinfector  who  does  not  act  in 
accordance  with  this  fact. 

4.  The  temperature  under  which  the  disinfecting  agent 
acts  influences  very  much  the  rapidity  and  the  certainty  of  its 
action.  Thus  Heider  found  that  anthrax  spores  that  survived 
the  action  of  a  five  per  cent  solution  of  carbolic  acid  thirty-six 
days  at  ordinarj-  room  temperature,  were  killed  in  from  one  to 
two  hours  at  131°  F.     Some  investigators  have  failed  to  state 


APPENDIX. 


DISINFECTION. 


^  300.      Disinfection,      By  disinfection  is  meant  the  des- 
truction of  infections  disease  producing  organisms.     For  this 
purpose,   nature    has    provided    very    important    agents   such 
as   sunlight   and   drying,  but  these   are  not   available  or  suffi- 
cient to  destroy  all  infecting  bacteria  in    all    infected   places 
within  the  necessary  time   limits.     To  supplement   these  nat- 
ural forces,  a  large  number  of  chemical  substances,  possessed 
of    germicidal    powers,  have  been    brought   into  service.      If, 
however,  the  results  of   the  test   experiments  with   these  dif- 
ferent substances  are  reviewed,  one  is  impressed  with  the  dis- 
crepancies, if  not  contradictory  conclusions,  recorded  concern- 
ing th'eir  value.      In  view  of  these  facts   the  practitioner  is 
often  at  a  loss  to  know  just  what  chemicals  to  use,   or  how  to 
apply  them  under  different  conditions  and  for  the  destruction 
of  different  species  of  organisms.     The  failure   resulting  from 
the  many  efforts  to  disinfect  stables,  pens,  kennels  and  yards 
has    caused    much    skepticism    concerning    the    efficiency    of 
many  reported  disinfectants.      In  order  to  rightly  understand 
the  reason  for  the  differences  in  results  of  the  test  experiments 
or  the  lack  of  uniformity  in  the  application  of  the  various  dis- 
infecting substances,    it  is  well  to  take  into  account  certain 
fundamental  facts. 

I.  The  bacteria  used  by  different  investigators  to  test  the 
efficiency  of  certain  substances  have  not  been  the  same.  The 
vital  resistance  of  the  various  species  is  very  different.  The 
results  obtained  in  testing  disinfectants  on  the  spirillum  of 
Asiatic  cholera  or  the  bacterium  of  bubonic  plague  give  but 
little  information  relative  to  the  value  of  the  same  disinfectants 
when  used  for  the  destruction  of  the  bacteria  of  glanders, 
tuberculosis  or  hog  cholera.     Thus  the  difficulty  in  accepting 


DISINFECTION 


371 


the  results  of  many  of  the  older  experiments  is  that  test 
organisms  were  used  which  are  very  unlike  those  for  which 
these  disinfectants  are  now  wanted.  The  practical  value  of 
the  more  recent  experiments  is  greater  because  they  have  more 
generally  dealt  with  species  of  bacteria  with  which  most  of  the 
work  of  disinfection  has  to  do. 

2.  The  power  of  resistance  of  the  same  species  of  bac- 
terium varies  greatly  under  different  conditions.  For  instance, 
Bear  found  that  a  freshh'  inoculated  culture  of  the  bacterium  of 
diphtheria  was  destroyed  with  i  :500o  of  nitrate  of  silver,  but 
that  a  twenty-four  hour  culture  required  i :  1000  of  the  same 
agent  to  kill  it  in  the  same  space  of  time.  In  some  work  done 
by  Esraarch  he  made  use  of  anthrax  spores  from  seventeen 
different  sources.  The}'  were  destroyed  b}-  steam  at  212°  F. 
in  from  one  to  twelve  minutes  and  by  a  five  per  cent  solution 
of  carbolic  acid  in  from  two  to  forty-two  days. 

3.  The  medium  in  which  the  bacteria  exists  influences 
the  results  of  the  disinfectants.  The  bacterium  of  tuberculosis 
from  an  aqueous  suspension  dried  upon  threads  may  be 
promptly  destroyed  by  mercuric  chloride,  but  in  fresh,  puru- 
lent, tuberculous  discharges  it  cannot  be  trusted  to  destroy- 
them.  Again  Behring  says  that  sporeless  anthrax  bacteria  in 
water  are  killed  by  corrosive  sublimate,  i  :  500,000  ;  in  bouillon, 
by  I  :  40,000  ;  but  in  blood  .serum  not  with  certainty  with  a 
solution  of  I  :  2000.  Some  disinfectants  are  influenced  very 
much  by  the  character  of  the  material  which  contains  the 
infectious  organism,  while  other  disinfectants  are  influenced  to 
a  comparatively  slight  degree.  The  experimental  work  which 
does  not  take  the  influence  of  the  media  upon  the  disinfectant 
into  account  is  not  of  much  practical  value  and  failures  are  to 
be  expected  in  the  work  of  the  disinfector  who  does  not  act  in 
accordance  with  this  fact. 

4.  The  temperature  under  which  the  disinfecting  agent 
acts  influences  very  much  the  rapidity  and  the  certainty  of  its 
action.  Thus  Heider  found  that  anthrax  spores  that  survived 
the  action  of  a  five  per  cent  solution  of  carbolic  acid  thirty-six 
days  at  ordinary  room  temperature,  were  killed  in  from  one  to 
two  hours  at  131°  F.     Some  investigators  have  failed  to  state 


372  DISINFECTION 

the  temperature  under  which   their   disinfecting  experiments 
were  made. 

5.  In  many  of  the  results  the  inhibitory  action  of  the 
agent  in  question  has  been  mistaken  for  its  germicidal  action. 
After  the  bacteria  have  been  subjected  to  the  influence  of  a 
disinfectant  for  a  given  time,  though  not  killed,  their  vege- 
tating and  pathogenic  capabilities  may  be  modified  but  still 
able,  under  favorable  conditions,  to  return  to  their  former 
vigor. 

The  rules  and  recommendations  of  the  various  cattle  com- 
missions and  those  having  authority  in  methods  for  prevention 
of  infectious  diseases  of  animals  do  not  very  clearly  define  the 
procedures  best  adapted  to  the  various  places  and  conditions 
requiring  disinfection.  The  many  chemicals  possessed  of 
germicidal  powers  and  the  numerous  commercial  disinfectants, 
recommended  largely  from  the  results  of  certain  definite  tests, 
which  in  point  of  fact  may  be  of  no  value  in  determining  their 
efficiency  for  the  conditions  in  question  render  further  inquiry 
into  the  best  methods  for  disinfecting  after  animal  diseases  a 
matter  of  much  scientific  interest  and  practical  value. 

§  301.  Conditions  to  be  taken  into  account  in  practi- 
cal disinfection.  In  the  effort  to  destroy  the  microorganisms 
in  such  places  as  yards,  stables,  cattle  cars  and  the  like,  it  is 
necessary  to  consider  before  applying  a  disinfectant  (i)  the 
resistance  of  the  particular  organism  to  be  destroyed,  (2)  the 
medium  in  which  it  exists,  (3)  the  nature  of  the  place  con- 
taining the  organisms  to  be  destroyed  and  (4;  the  chemical 
action  of  the  material  surrounding  the  microorganisms  on  the 
disinfectant  itself.  If  the  disinfection  is  for  anthrax  or  Texas 
fever  (cattle  tick)  a  more  powerful  substance  or  solution  must 
be  employed  than  would  be  required  in  disinfecting  for  the 
bacteria  of  septicaemia  hemorrhagica.  If  the  infecting  organ- 
isms are  mixed  with  fecal  matter,  dirt  or  fodder,  the  problem 
is  a  different  one  than  where  they  rest  on  a  comparatively  clear 
surface.  It  matters  again  whether  the  infecting  organisms  are 
in  the  soil  (on  surface),  on  a  stable  floor  that  is  tight  and  hard 
or  on  one  containing  cracks  of  various  sizes  and  made  up  ot 
board,  more  or  less  shattered  or  decayed,  thus  furnishing  deep 
recesses  for  the  hiding  away  as  it  were  of  the  specific  organisms. 


DISENFECTION 


37: 


In  the  disinfection  of  human  dwellings  the  fumigation 
with  formaldehj-de  has  proven  to  be  one  of  the  cheapest  and 
ordinarily  the  most  efficient  procedures,  but  it  requires  a 
tight!}-  closed  room.  It  is  evident  that  such  a  method  cannot 
be  trusted  for  the  disinfection  of  most  barns,  stalls  or  stables 
which  are  usualh-  both  large,  compared  with  dwelling  rooms, 
and  what  is  of  far  more  importance  too  open.  For  the  disin- 
fection from  animal  diseases  the  agents  used  must  in  most  cases 
be  applied  in  the  form  of  a  solution. 

Jaeger's  investigations  brought  out  ver\'  clearly  the  neces- 
sity of  adapting  the  disinfecting  agent  to  the  specific  kind  of 
infection  to  be  destroyed.  For  instance,  while  brushing  the 
surface  with  a  i  :  3  milk  of  chloride  of  lime  destroyed  anthrax 
spores,  it  was  untrustworthy  as  a  disinfectant  for  the  bacteria 
of  tuberculosis  and  of  glanders.  For  the  destruction  of  the 
bacterium  of  tuberculosis  he  found  carbolic  acid  and  the  other 
coal-tar  phenols  very  efficient,  especially  wdien  acidulated  with 
hydrochloric  acid.  For  this  purpose  he  recommended  espe- 
cially Laplace's  4  per  cent  solution  of  crude  carbolic  acid  with 
two  per  cent  of  hydrochloric  acid.  In  the  hands  of  Jaeger, 
the  power  to  destroy  anthrax  spores  with  certainty  has  been 
shown  only  by  solutions  of  carbolic  acid  and  the  thick  chloride 
of  lime  mixture. 

A  thick  milk  of  lime  applied  once  with  a  brush,  Jaeger 
found  efficient  in  the  destauction  of  the  microorganisms  of 
chicken  cholera, hog  cholera,  erysipelas  of  swine,  typhoid  fever, 
glanders,  anthrax  bacillus  without  spores  and  staphylococcus 
pyogenes  aureus. 

Giaxa,  in  a  similar  line  of  work  to  that  of  Jaeger's,  found 
that  in  the  disinfection  of  walls  even  a  five  per  cent  lime  wash 
acting  forty-eight  hours  failed  to  destroy  anthrax  spores,  the 
bacterium  of  tuberculosis  and  the  bacillus  of  tetanus. 

A  strong  soltition  of  the  chloride  of  lime  may  be  classed 
as  one  of  the  rapidly  acting  disinfectants  for  most  bacteria,  but 
Jaeger's  report  of  its  failure  when  applied  to  the  infection  of 
tuberculosis  and  glanders  should  be  borne  in  mind.  For  the 
cleansing  of  cattle  cars  Gruber  advises  scrubbing  them  out 
with  hot  water  or  washing  with  a  two  per  cent  solution  of  soda 


374  DISENFECTION 

at  50°  C,  although  this  has  no  particular  disinfecting  power. 
If  the  cars  are  infected  he  sprays  with  a  5  to  10  per  cent  solu- 
tion of  formaldehyde. 

For  disinfecting  pens,  stable  floors  and  the  like  the  follow- 
ing solutions  have  been  recommended  and  their  careful  and 
intelligent  use  has  shown  them  to  be  very  efficacious. 

1.  Cort'osivc  sublimate  {mejxui'ic  chloride) ,  i  ounce  in  8 
gallojis  of  zvater  {one-tenth  of  i per  cent).  The  water  should  be 
put  into  wooden  tubs  or  barrels  and  the  powdered  sublimate 
added  to  it.  The  whole  must  be  allowed  to  stand  for  twenty- 
four  hours,  so  as  to  give  the  sublimate  an  opportunity  to  be- 
come entirely  dissolved.  Since  this  solution  is  poisonous,  it 
should  be  kept  covered  up  and  well  guarded.  It  may  be  ap- 
plied with  a  broom  or  mop  and  should  be  used  freely  on  all 
woodwork .  Since  it  loses  its  virtue  in  proportion  to  the  amount 
of  dirt  present,  all  manure  and  other  dirt  should  be  first 
removed  before  applying  the  disinfectant.  The  manure  should 
be  covered  with  lime. 

2.  Chlorinated  lime.  Five  ounces  of  chloride  of  lime  to  a 
gallon  of  water  (4  per  cent).  This  should  be  applied  in  the 
same  wa}'  as  the  corrosive  sublimate. 

3.  A  mixture  of  crude  carbolic  and  sulphuric  acids.  The 
following  disinfectant  has  been  found  to  be  very  serviceable. 
It  is  not  poisonous,  but  quite  corrosive,  and  care  should  be 
taken  to  protect  the  eyes  and  hands  from  accidental  splashing  : 

Gallon. 

Crude  carbolic  acid ^ 

Crude  sulphuric  acid .|< 

These  two  substances  should  be  mixed  in  tubs  or  glass 
vessels.  The  sulphuric  acid  is  ver}-  slowly  added  to  the  car- 
bolic acid.  During  the  mixing  a  large  amount  of  heat  is  de- 
A' eloped.  The  disinfecting  power  of  the  mixture  is  heightened 
if  the  amount  of  heat  is  kept  down  b}'  placing  the  tub  or  glass 
demiiohn  containing  the  carbolic  acid  in  cold  water  while  the 
sulphuric  acid  is  being  added.  The  resulting  mixture  is 
added  to  w^ater  in  the  ratio  of  i  to  20.  One  gallon  of  mixed 
acids  will  thus  furnish  20  gallons  of  a  strong  disinfecting  solu- 
tion, having  a  slightly  milky  appearance. 


DISENFECTION  375 

4,  Ordinary  slaked  lime,  though  it  does  not  possess  the 
disinfecting  power  of  the  substances  given  above,  is  neverthe- 
less very  useful,  and  should  be  used  more  particularly  on  in- 
fected soil. 

More  recently  the  thorough  sprinkling  of  the  floors,  walls, 
and  ceilings  with  Formalin  has  been  highly  recommended. 

In  disinfecting  stables  and  pens  all  litter  which  has  accu- 
mulated should  be  'removed  before  applying  the  disinfectant. 
As  the  litter  itself  is  infected  it  should  be  disinfected  as  well  as 
the  stable,  floor  and  walls.  The  most  eflicient  method  for  this 
is  fire.  The  practice  of  washing  the  floors  and  ceiling  with 
water  before  applying  the  disinfectant  has  in  most  instances 
the  disadvantage  that  the  water  carries  the  microorganisms  to 
be  destroyed  into  cracks  and  possibly  through  the  floor  where 
they  will  not  be  affected  by  the  later  application  of  the  germi- 
cide. It  is  deemed  safer,  to  simply  use  a  dry  cleaning  in 
which  the  sweepings  are  burned  and  then  apply  the  disinfect- 
ant in  sufficient  quantities  to  thoroughly  saturate  the  surfaces 
including  the  adhering  particles  of  dirt.  The  solutions  avail- 
able for  stable  disinfection  are  cheap  enough  to  admit  of  this 
precaution. 

It  is  often  desirable  to  disinfect  yards  where  infected 
animals  have  been  kept.  It  is  well  in  such  cases  to  carefully 
scrape  together  and  burn  the  litter  after  which  the  surface  of 
the  soil  must  be  disinfected.  For  this  the  milk  of  lime  or  a 
a  very  liberal  coating  of  slacked  lime  has  been  recommended. 
The  burning  of  the  surface  as  can  be  done  by  covering  it  with 
a  layer  of  old  straw  and  burning,  is  a  more  certain  destroyer, 
especially  if  animal  parasites  are  to  be  eliminated.  The  method 
of  disinfecting  with  a  flame  as  described  by  Ferbusch  in  1896 
and  recently  recommended  by  Stiles  for  disinfecting  kennels, 
pens  and  yards  offers  possibilities  not  found  in  other  means. 
The  procedure  consists  of  a  "Cyclone  burner"  attached  to  the 
end  of  a  long  iron  tube  with  a  wooden  shield.  This  is  con- 
nected with  a  short  piece  of  hose  of  the  kind  made  for  the 
delivering  of  oil  attached  to  a  spray  pump.  A  tank  of  suitable 
size  is  taken  and  paraffin  gas  oil  is  used-.  The  spray  of  oil  is 
ignited  giving  a  very  hot  and  effective  flame  which  is  run  over 


376  DISENFECTION 

the  surface  to  be  disinfected.  The  fianie  destroys  all  living' 
things  on  the  surface.  This  method  seems  to  be  applicable  to 
the  disinfection  of  floors  and  stables  as  well  as  yards,  when 
the  conditions  are  permissible  and  when  the  flame  can  be 
applied  with  the  necessary  care.  Experiments  are  being  made 
to  determine  more  definitely  the  extent  to  which  this  method 
can  be  applied  with  safety. 

REFERENCES. 

1.  RiDEAL.     Disinfectants  and  disinfection.     London.      1895. 

2.  Stiles.     The  disinfection  of  kennels,  Pens   and  yards  by  fire. 
Bulletin  No.  j^,  U.  S.  Bureau  of  Animal  Industry.     1902.     p.  15. 

3.  Young.     Notes   on   disinfectants   and    disinfection.     Reprinted 
from  the   loth   Report  oj   the  State   Board  of  Health   of  Maine.     1898. 

(Contains  full  bibliography  on  disinfectants  and  results  of  experiments. ) 


INDEX. 


Actinomycosis,  204. 

Characterization,  204. 

Differential  diagnosis,  215. 

Etiology,  206. 

Geographical  distribution,  205. 

History,  204. 

Infection,  207. 

Morbid  anatomy,  209. 

Sanitary  considerations,  216. 

Specific  treatment,  216. 

Symptoms,  208. 
Amoeba  dysenteriae,  256. 
Amoeba  meleagridis,  254. 
Animal  inoculation,  123,  151. 
Animal    parasites,  diseases  caused 

by,  355- 
Anthrax,  81. 

Animals  attacked,  85. 

Channels  of  infection,  85. 

Characterization,  81. 

Differential  diagnosis,  93. 

Disposition  of  animals  dead  of 
anthrax,  97. 

Etiology,  83. 

Geographical  distribution,  82. 

History,  82. 

Morbid  anatomy,  90. 

Pasteur's  anthrax  vaccine,  95. 

Protective  inoculation,  94. 

Symptoms,  87. 

Toussaint's  anthrax  vaccine, 96. 
Law's  modification   of,  96. 
Apoplectiform  septicsemia  in  chick- 
ens, 44. 

Characterization,  44. 

Differential  diagnosis,  46. 

Etiology,  44. 

Geographical    distribution,  44. 

History,  44. 

Morbid  anatomy,  45. 

Prevention,  46. 

Symptoms,  45. 
A  specific  infectious  disease,  3. 
Aspergillus ficniigatus,  230. 
Asthenia  in  fowls  and  pigeons,  167. 

Characterization,  167. 

Etiolog}-,  167. 

History,  167. 

Morbid  anatomy,  168. 

Symptoms,  168. 


Bacillus  choletrc  suis,  171,  181. 

Brief  description  of,  171. 
Bacillus  cloaca;,  351. 
Bacillus  tetaui,  186. 
Bacteria  causing  wound  infection, 6. 
Bacterium  anthracis,  83. 
Bacterium  asthenics,  167. 
Bacterium  of  swine  plague  181. 
Bacterium  septiccsniiae  heniorrhag- 

icae,  48,  70. 
Bacterium  tuberculosis,  131. 

Cultivation  of,  131. 
Black  head  (See  infectious  entero- 

hepatitis). 
Boophilis  bovis,  241. 
Botryomycosis,  7. 

Cerebro-spinal  meningitis  (See  in- 
fectious    cerebrospinal 
meningitis). 
Channels  of  infection,  4. 

Through  abrasions  of  skin,  5. 
"  agency  of  insects,  5. 

"  digestive  tract,  4. 

"  generative  organs,  5. 

"  respiratory  tract,  5. 

"  transmission     from 

parent  to  foetus,  5. 
Contagious    pleuro-pneumonia    in 
cattle,  290. 
Characterization,  290. 
Differential  diagnosis,  299. 
Eradication,  301. 
Etiology,  293. 
History,  290. 
In  the'U.  S.,  291. 
Morbid  anatomy,  296. 
Preventive  inoculation,  301. 
Symptoms,  294. 
Cornstalk  disease,  349. 
Characterization,  349. 
Differential  diagnosis,  354. 
Etiology,  352 

Geographical  distridution,  351. 
History,  350. 
Morbid  anatomy,  353. 
Symptoms,  352. 
Davainae  tetragona,  361. 
Diarrhoea     in     calves    (See    white 

scours) 
Diphtheria  in  fowls,  325. 


378 


INDEX 


Characterization,  325. 

Etiology,  326. 

History,  326. 

Morbid  anatomy,  328. 

Prevention,  332. 

Relation  to  human  diphtheria, 
330. 

Symptoms,  327. 
Disinfectants,  374. 
Disinfection,  370. 
Dog  distemper,  340. 

Characterization,  340. 

Differential  diagnosis,  346. 

Etiology,  340. 

Geographical  distribution,  340. 

History,  340. 

Morbid  anatomy,  344. 

Prevention,  347. 

Symptoms,  341. 
Dourine.  272,  274. 

Characterization,   274. 

Etiology,  274. 

History,  274. 

Morbid  anatomy,  278. 

Prevention,  281. 

S3'mptoms,  276. 
Equine     contageous    pleuro-pneu- 
monia,  37. 

Characterization,  37. 

Differential  diagnosis,  44. 

Etiology,  38. 

Geographical  distribution,  37. 

History,  37. 

Morbid  anatomy,  4r. 

Symptoms,  40. 
Etiology,  I. 
Farcy  (See  glanders). 
Fistulous  withers,  15. 
Foot  and  mouth  disease,  302. 

Characterization,  302. 

Differential  diagnosis,  306. 

Etiology,  303. 

Geographical  distribution,  303. 

History,  303. 

Morbid  anatomy,  305. 

Prevention,  306. 

S3'niptoms,  303. 
Fowl  cholera,  77 

Characterization,  77. 

Differential  diagnosis,  80/ 

Etiology,  78' 

Geographical  distribution,  78. 

History,  77. 

Morbid  anatomy,  79. 

Prevention,  8r. 

Symptoms,  78. 


Glanders,  1 13. 

Characterization,  113. 

Differential  diagnosis,  122. 

Etiology,  115. 

Geographical  distribution,  114. 

Glanders  in  man,  121. 

Historj',  1 13. 

Morbid  anatomy,  117. 

Symptoms,  1 15. 
Hemorrhagic  septicaemia  in  cattle, 
68. 

Characterization,  68. 

Differential  diagnosis,  76. 

Etiology,  70. 

Geographical   distribution,  70. 

History,  68. 

Morbid  anatomy,  72. 

Prevention,  76. 

Symptoms,  71. 
Hog  cholera,  169. 

Characterization,  169. 

Differential  diagnosis,  180. 

Etiology,  171. 

Geographical  distribution,  171. 

History,  ]69. 

Morbid  anatomy,   J75. 

Prevention,  182. 

Specific  treatment,  184. 

Symptoms,  T74. 
Infection,  2. 

Infectious     cerebro-spinal    menin- 
gitis, 347; 

Characterization,  347. 

Etiology, 347. 

Morbid  anatomy,  349. 

Symptoms,  348. 
Infectious  entero-hepatitis,  252. 

Characterization,  252. 

Differential  diagnosis,  264. 

Etiology,  254. 

Geographical  distribution,  253. 

History,  253. 

Morbid  anatomy,  257. 

Post-mortem  notes,  263. 

Prevention,  264. 

Symptoms,  256 
Infectious  leukaemia  in  fowls,  98. 

Characterization,  98. 

Differential  diagnosis,  105. 

Etiology,  99 

Geographical   distribution,  98. 

History,  98. 

Morbid  anatomy,  loi. 

Symptoms,  99. 
Infectious  mastitis,  15. 

Bacteria  of,  18. 


INDEX 


379 


Infectious    pneumonia     in     swine 

(See  swine  plague). 
Influenza,  334. 

Characterization,  334. 

Differential  diagnosis,  339. 

Etiology,  335. 

Geographical  distribution,  335. 

History,  335. 

INIorbid  anatomy,  338. 

Symptoms,  336. 
Leeches,  218. 

Characterization,  218. 

Etiology,  221. 

Geographical  distribution,  221. 

History,  220. 

Morbid  anatomy,  222. 

Treatment,  228. 
Mai  dc  cadt'ras,  273. 
Mallein,  123. 

Micrococcus  lauceolafus,  48. 
Migula's      classification      of      bac- 
teria, 25. 
Nagana,  272. 

Nodular  disease  in  cattle,  360. 
Nodular  disease  of  sheep,  355. 

Characterization,  355. 

Differential  diagnosis,  259. 

Etiology,  356. 

Geographical  distribution,  355. 

History,  355. 

Morbid  anatomy,  356. 

Prevention,  359. 
Normal  temperature  of  cattle,  156. 

Effect  of  drinking  wateron,  157. 
CEsophai^ostoma        Columbianum, 

'356. 
Omphalophlebitis,  8. 
Ovine  caseous  lymph  adenitis,  161. 

Characterization,  161. 

Differential  diagnosis,  166. 

Etiology,  162. 

Geographical  distribution,  162. 

Historv,  161. 

Morbid  anatomy,  163. 

Symptoms,  162. 
Pleuro-pneumonia  ( See  contagious 

pleuro-pneumonia. 
Pneumomycosis,  228. 

Morbid  anatomy,  231. 

Species  of  fungi,  228. 
Poll  evil,  15. 

Practical  disinfection,  372. 
Pyroplasma  bigeiiiiniim,  238. 
Pyrosoma  higeminum,  238. 
Rabies,  306 

Differential  diagnosis,  320. 


Etiology,  308. 

Geographical  distribution,  307. 

History,  307. 

Method  of  invasion,  309. 

Morbid  anatomy,  315. 

Period  of  incubation,  3T0. 

Prevention,  324. 

Symptoms,  312. 

Treatment,  324. 
Ray  fungus,  206, 
Rinderpest,  282. 

Characterization,  282. 

Differential  diagnosis,  287. 

Etiology,  283. 

Geographical  distribution,  2S3. 

History,  282. 

Morbid  anatomy,  285. 

Prevention,  287. 
Septicaemia,  3. 
Specific  infectious  disease,  19. 

Cause  of  variation  in,  22. 

Differential  characters  of,  20. 

Grouping_^of,  22. 
Strangles,  33. 

Characterization,  33. 

Differential  diagnosis,  36. 

Etiology,  34. 

Geographical  distribution,  33. 

History,  33. 

Morbid  anatomy,  35. 

Symptoms,  34. 
Streptococci,  27. 

Classification  of,  29. 

Diseases  due  to,  27. 

Distribution  in  nature,  30. 

General  discussion  of,  27. 
Surra,  265. 

Characterization,  265. 

Differential  diagnosis,  272. 

Etiolog}',  266. 

Geographical  distribution,  265. 

Historv,  265. 

Morbid  anatomy,  268. 

Prevention,  272. 

Report  of  Smith  and  Kinyoun, 
269. 

Symptoms,  267. 
Swine  erysipelas,  107. 

Characterization,  107. 

Differential  diagnosis,  in. 

Etiology,  108. 

Geographical  distribution,  107. 

Morbid  anatomy,  109. 

Preventive  inoculation,  in. 

Symptoms,  108. 
Swine  plague,  47. 


38o 


INDEX 


Autopsy  notes,  59. 

Bacterium  of,  50. 

Characterization,  47. 

Differential  diagnosis,  61. 

Etiology,  48. 

Geographical    distribution,  48. 

History,  47. 

In  rabbits,  63. 

Modification  of  in  rabbits,  64. 

Morbid  anatomy.  52. 

Prevention,  62. 

Specific  treatment,  63. 

Symptoms,  52. 
Symptomatic  anthrax,  195. 

Characterization,  195. 

Differential  diagnosis,  200. 

Etiology,  196 

Geographical  distribution,  196. 

History,  195. 

Morbid  anatomy,  198.* 

Prevention,  201. 

Preventive  inoculation,  202. 

Symptoms,  197. 
Tcrniif  dot/in'op/ihs(See  Davainae ) . 
Tfeniasis  in  fowls,  360. 

Characterization,  360. 

Differential  diagnosis,  363. 

Etiology,  361. 

Geographical  distribution,  361. 

History,  361. 

Morbid  anatomy,  361. 

Symptoms,  361. 
Tetanus,  185. 

Characterization,  185, 

Differentia]  diagnosis,  192. 

Etiology,  186. 

Geographical  distribution,  185. 

History,  185. 

Mode  of  infection,  187. 

Morbid  anatomy,  190. 

Prevention,  193. 

Symptoms,  188. 
-    ,  Tetanus  antitoxin,  193. 
Texas  fever,  236. 

Characterization,  236. 

Differential  diagnosis,  249. 

Etiology,  238. 

Geographical  distribution,  237. 


History,  236. 

Immunizing  susceptible  cattle, 
249. 

Infection,  240. 

Morbid  anatomy,  245. 

Prevention,  249. 

Symptoms,  244. 
Toxaemia,  3. 
Trichinosis,  364. 

Characterization,  364. 

Description  of  T.  spirallis,  364. 

Diagnosis,  368. 

Frequency,  366. 

History,  364. 

Manner  of  infection,  366. 

Morbid  anatomy,  368. 

Prevention,  369. 

Symptoms,  367. 
Trypanosoma  Brucei,  272. 
"  eqiiinum,  273. 

"  eqjiiperdnm,  272. 

"  Evansi,  266. 

"  Lewis,  273. 

Trypanosomiasis,  272. 
Tse  tsefl  y  disease,  272. 
Tuberculin,  151,  235. 

Application  of,  154. 

Preparation  of,  152. 
Tuberculosis,  127. 

Characterization,  127. 

Differential  diagnosis,  150. 

Etiology,  131. 

Extent  of  in  cattle  and  swine, 
129. 

Geographical  distribution,  130. 

History,  127. 

Local  and  generalized,  144. 

Morbid  anatomy,  137. 

Prevention,  158. 

Symptoms,  133. 

Tuberculosis  in  swine,  144. 
Symptoms,  147. 
Morbid  anatoni}',  148. 
White  scours  in  calves,  10. 

Nocard's  treatment  of,  12. 
Wound  infection,  3,  6. 

Bacteria  causing,  6. 


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